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JULY 1 998 

VOLUME 43 

NUMBER 7 

ISSN 0020-1324-RECACP 



RE/PIRATORy 



j^ 



44* International Respiratory Congress 
November 7-10, 1998 • Atlanta, Georgia 



A MONTHLY SCIENCE JOURNAL 
43RD YEAR— ESTABLISHED 1956 



EDITORIALS 



Professionalism, Respiratory Care Practice, and 
Physician Acceptance of a Respiratory Consult Service 

ORIGINAL CONTRIBUTIONS 

Medical House Staff Impressions of a 
Respiratory Therapy Consult Service 

Two-Tiered Response for Emergency Airway 
Management by Respiratory Therapists and 
Anesthesiologists 

Acute Pulmonary Effects of Toxic 
Nitrogen Dioxide Fume Inhalation 



CASE REPORTS 



Intractable Wheezing Due to an Obstructing 
Tracheal Neuroendocrine Tumor in an Adolescent 
with HIV Infection 



A TRIBUTE TO JOHN H EMERSON 



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ALSO 
IN THIS ISSUE 


1 


AARC Membership 
595 Application 




Abstracts from 
526 Other Journals 




Advertisers Index 
600 & Help Lines 




Author 
600 Index 




Calendar 
597 of Events 




Manuscript 
591 Preparation Guide 




589 MedWatch 




New Products 
585 & Services 




598 Notices 




RE/PIRATORy 
QiRE 




A Monthly Science Journal 
Established in 1956 

The Official Journal of the 

American Association for 

Respiratory Care 



JULY 1998 / VOLUME 43 / NUMBER 7 



EDITORIALS 



Professionalism, Respiratory Care Practice, and 
Physician Acceptance of a Respiratory Consult Service 

/ly Deem R Hess — Bosum. Massachusetts 



ORIGINAL CONTRIBUTIONS 



CASE REPORTS 



A TRIBUTE TO JOHN H EMERSON 



546 



Medical House Staff Impressions Regarding the Impact 
of a Respiratory Therapy Consult Service 

by James K Stoller and Irene Michnicki — Cleveland. Ohio 

Two-Tiered Response for Emergency Airway Management 
by Respiratory Therapists and Anesthesiologists 

by John D Hiissey. Michael J Bishop. Le»is Massey. S Uikshminaraxun. 
James Joy. and Jennifer Finley — Seattle. Washington 

Acute Pulmonary Effects of Toxic Nitrogen Dioxide 
Fume Inhalation 

h\ Dhcerai (iiipta. Ashutosh Nath Aggarwal, Sanjay Jain. 
nii;ainhcr Kchcra. and Surinder Kumar Jindal — Chandigarh, India 



549 
552 
557 



Intractable Wheezing Due to an Obstructing Tracheal 
Neuroendocrine Tumor in an Adolescent with HIV Infection 

by Shari Eason Ludlam. David Zeldman. Ltniren V Wood, and 
Frederick P Ognibene — Bethesda. Mankind 



562 



Jack Emerson; Notes on His Life and Contributions 
to Respiratory Care 

by Richard D Branson — Cincinnati. Ohio 

Some Reflections on the Man Behind the Machines 

by James K Stoller — Cleveland. Ohio 

Some Reflections on Iron Lungs and Other Inventions 

the transcript of a lecture by John H Emerson 

Artificial Respiration in the Treatment of Edema of 

the Lungs: A Suggestion Based on Animal Experimentation 

by Haven Emerson — New York. New York 

Reprinted, with Permission, from Arch Intern Med I909:3:36H-37I 



567 
572 
573 

583 





Keep moving. 



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pills k(\ word sea re lies of all availalilc issues. Don I I'oi'i^cl llie ( )Mline Kesoiirees seel ion: \oii can eon- 
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RE/PIRATORy CtRE 

Rrow.sc snCclx. 



EDITORIAL OFFICE 




EDITOR IN CHIEF 



Respiratory Care iiSSN 0020-1324, USPS 0489- 
190) IS published monthly by Daedalus Enterprises Inc, at 
1 1030 Abies Lane. Dallas TX 75229-4593. for ihe Amer- 
ican Association for Respiratory Care, One volume is 
published per year beginning each January. Subscription 
rates are $75 per year in the US; $90 in all other countries 
(for airmail, add $94). 

The contents of the Journal are indexed in Hospital and 
Health Administration Index. Cumulative Index to Nurs- 
ing and Allied Health Literature. EMBASE/Exerpta Med- 
ica, and RNdex Library Edition, Abridged versions of 
Respiratory Care are also published in Italian. 
French, and Japanese, with permission from Daedalus En- 
terprises Inc. 

Periodicals postage paid at Dallas TX and at additional 
mailing offices, POSTMASTER: Send address changes lu 
RESPIRATORY CARE. Membership Office. Daedalus En 
terpnses Inc. 1 1030 Abies Lane, Dallas TX 75229-4593. 
Primed in the United Stales of America 
Copyright © 1998. hy Daedalus Enterprises Inc. 



David J Pierson MD 

Harhoniew Medical CciUci 
Uf}iversin- of Washi/i,i>fon 
Seattle. Washington 



ASSOCIATE EDITORS 



Richard D Branson RRT 

Universily of CincinnaU 
Cinciiiiuili. Ohio 



Charles G Durbin Jr MD 

University of Virginia 
CharlottesviUe. Virginia 

EDITORIAL BOARD 



Dean R Hess PhD RRT 

Massachusetts General Hospital 
Harvard University 
Boston. Massachusetts 

James K StoUer MD 

Tlw Cleveland Clinic Foundation 

Cleveland. Ohio 



Thomas A Barnes EdD RRT 
Northeastern University 
Boston. Masstichusetts 

Michael J Bishop MD 
University of Washington 
Seattle. Washington 

Bartolome R Celli MD 

Tufts Universux 
Boslon. Mas.mclnisells 

Robert L Chatbum RRT 

University' Hospitals of Cleveland 
Case Western Reseire University 
Cleveland. Ohio 

Luciano Gattinoni MD 

Universit\' of Milan 
Milan. Italy 

John E Heffner MD 

University of Arizona 
Phoenix. Arizona 

Mark J Heulitt MD 

University' of Arkansas 
Little Rock. Arkansas 



SECTION EDITORS 



Leonard D Hudson MD 
University of Washington 
Seattle. Waslwii^lon 

Robert M Kacmarek PhD RRT 
Massachusetts General Hospital 
Harx'ard University 
Boston. Xfassachusetts 

Toshihiko Koga MD 
Koga Hospital 
Kiirunie. Japan 

Marin H Kollef MD 
Washington University 
St Louis. Missouri 

Patrick Leger MD 

Ctinique Medicate Edouard Rist 



Neil R Maclntyre MD 
Duke University 
Durham. North Carolina 

John J Marini MD 
University of Miimesota 
St Paul. Minnesota 



Shelley C Mishoe PhD RRT 

Medical College of Georgia 
Augusta. Georgia 

Joseph L Rau PhD RRT 
Georgia Stale University 
Atlanta. Georgia 

Catherine SH Sassoon MD 
University of California hrine 
Long Beach. California 

Arthur S Slulsky MD 
University of Toronto 
Toronto. Ontario, Canada 

Martin J Tobin MD 

Loyola University 
Maywood. Illinois 



STATISTICAL CONSULTANT 

Gordon D Rubenfeld MD 

University of Washington 
Seattle. Washington 



Robert R Fluck Jr MS RRT 
MS Jastremski MD 
Blood Gas Corner 



Hugh S Malhewsi 
Drug Capsule 



Charles G Irvin PhD 

Gregg L Ruppel MEd RRT RPFT 

PFT Corner 



Richard D Branson RRT 
Robert S Campbell RRT 
Kittredge 's Comer 



Jon Nilsesiucn PhD RRT 
Ken Hargcll RRT 
Robert Harwood MSA RRT 
Graphics Corner 



Patricia Ann Doorley MS RRT 
Charles G Durbin Jr MD 
Test Your Radiologic Skill 



Barbara Wilson MEd RRT 
Jon Meliones MD 
John Palmisano RRT 
Cardiorespiratory Interactic 



CONSULTING EDITORS 



Frank E Biondo RRT 
Howard J Birenbaum MD 



Donald R Elton MD 
Ronald B George MD 



James M Hurst MD 
Michael McPeck RRT 



John Shigeoka MD 
Jeffrey J Ward MEd RRT 



Abstracts 



Summaries of Pertinent Articles in Other Journals 



Editorials, Commentaries, & Reviews To Note 

Life-Support System Benefits from Noise — Suki B. Alenc:ir AM. Sujeer MK. Lutchen KR, roliins 
JJ. AniirudeJSJr. elLil. Nature IWS;393(6681): I27-I2S. 

The Knd-of-I,ife Sequence (Revieul—Waisel DB, Tniog RD. Anesthesiology I997;87(3):676-(S86. 

Case 30-1997: Pulmonary Interstitial Empiiysema in Infancy (Letter) — Fox RB, Wright AM 
NEnglJ Med IW8;33S( 10):6S8. 

Case 30-1997: Pulmonary Interstitial Emphysema in Infancy (Letter) — Lefehvre F. N Engl J Med 
l998;33S(in):688-689. 

Non-steroidal Anti-Inflammatory Therapy for Asthma (Letter) — Kon OM, Robinson DS. Lancet 
I998;35l(9103):672. 

Prognosis of ARDS Patients: Light at the End of the Tunnel? (Editorial) Steltzer H. Krafft P. 
Intensive Care Med l997:23(S):803-8()5. 

Staffing ICUs: The Good News and the Not-So-Cood News (Editorial )— Barash PG, Rosenhaiim 
SH. Chest I998;l l3(3);569-57(). 

Multiple-Breath Nitrogen Washout Techniques: Including Measurements with Patients on Ven- 
tilators— Newth CJ. Enright P. Johnson RL. Eur Respir J I997;I0(9):2I74 218?. 

Roentgen, Tourette, Angstrom, Bechterew, and Other Misspelled Names (Letter) — Navarro FA. 
Lancet 1998;35l(9in3):682. 

Inhaled Nitric Oxide: ,\ Tenth Anniversary Observation — Truog WE. Pediatrics 1998:101(4 Pt 

1 ):696-697. 

Noninvasive Ventilatory Support — Saving a Life without Intubation — Birnbaumer DM. West 
J Med I998;I68(3):I82-I83. 



Predictors of Quality of Life and Adjustment 
after Lung Transplantation — Cohen L. Lit- 
tlefield C. Kelly P. Maurer J. Abbey S. Chest 
I998;1I3(3);633. 

OBJECTIVE: Few studies have examined pre- 
dictors of quality of life and adjustment after lung 
transplantation. This study determined whether 
pretransplant psychological measures predicted 
physical health, quality ol life, and overall adjust- 
ment post-transplant. Cross-sectional analyses also 
examined differences in adjustment and quality 
of life for lung transplant candidates and recip- 
ients. niiSICN &. PARTICIPANTS: Seventeen 
transplant candidates and 60 transplant recipients 
completed questionnaires measuring adjustment 
and quality of life. In addition, we examined 
archival data on 107 transplant candidates who 
had received pretransplant psychological assess- 
ments, and post-transplant physical health status 



data were collected on these patients. Ollhe 107 
patients who provided a pretransplant psycho- 
logical assessment, 32 completed the question- 
naires measuring post-transplant adjustment and 
quality of life. SETTING: University medical cen- 
ter transplant service. RESULTS: Cross-sectional 
analyses indicated significantly better adjustment 
and quality of life post-transplant. Pretransplant 
psychological variables were not associated with 
measures of posi-iransplant physical health. Hier- 
archical multiple regression analyses found that 
pretransplant anxiety and psychopalhology pre- 
dicted post-transplant adjustment (/3s ranging from 
0.32 to 0.68) and greater pretransplant anxiety 
also predicted worse post-transplant quality of life 
(/Js ranging from 0.29 to 0.62). Subjective sleep 
disturbances were associated with poorer adjust 
ment and quality of life (fh ranging from 0.36 lo 
0.7.S), and were found to mediate the relationship 
between presurgical anxiety and post-transplaiii 



adjustment and quality of life. CONCLUSIONS: 
This study found that psychological status pre- 
transplant predicted adjustinent and quality of life 
post-transplant. Moreover, increased anxiety lev- 
els pretransplant predicted subsequent subjective 
sleep disturbances, which were, in turn, associ- 
ated with poorer adjustment and quality of life. 
The benefits of pretransplant stress management 
interv entions are discussed. 

Compliance with National .\slhma Manage- 
ment (Guidelines and Specialty Care: A Health 
Maintenance Organization Experience — Iji'gor- 
reta AP, Christian-Herman J, O'Connor RD, 
Hasan MM. Evans R, Leung KM. Arch Intern 
Med l998:l.<i8(.S):4,S7. 

BACKGROUND: fo improve asthma disease 
nianagemenl, the National Asthma Education Prcv 
giam (NAEP) Expeil Panel published (iuklelhus 



'Sib 



RESPIRATORY CARF. 'JULY I W8 VOL 4.^ NO 7 




YOU'D BE SURPRISED WHAT NEW EASIVENT" WILL HOLD. 





And so will your patients. 

Any holding chamber will hold a dose of respiratory 
medication. But only the EasiVent" Valved Holding Chamber 
is designed to hold the complete MDI kit inside. Or any 
other personal treasure of modest size. 

■'~^ Physicians, respiratory therapists, and patients indicate a preference for the 

unique design of EasiVent'".* Since EasiVent'^' improves the portability of asthma 
treatment, it encourages patient compliance. 

NAEPP guidelines also recommend that all patients using corticosteroids use 
a holding chamber to maximize dose delivery. Which is exactly what EasiVent™ is 
designed to do. 

EasiVent" improves medication delivery and simplifies patient training, with 
advanced features such as a dual, low-resistance valve, universal MDI port, graphic 
instructions printed on the unit, and built-in coaching signal. 

Help your patients with compliance. Specify the EasiVent'" Valved Holding Chamber. ^ 

It not only holds the complete MDI kit inside, its advanced design also helps the patient 
get maximum benefit from their medication. And that's no fish story. -n^.^ on file 

Circle 102 on reader service card 



DE]^ 



^1998 DEY, 
All rights reserved. 
09-527-00 5/98 



Abstracts 



for the Diagnosis and Manugement ofAslhimi in 
1 99 1 . OBJECTIVES: To compare the current sta- 
tus of asthma disease management among patients 
in a large health maintenance organization with 
the NAEP guidehnes and to identify the factors 
that may be associated with medical care (eg, 
emergency department visits and hospital admis- 
sions) and adherence to the guidelines. METH- 
ODS: Analyses of 1996 survey data from 5.580 
members with asthma (age range, 14 to 65 years) 
covered by a major health maintenance organi- 
zation in California (Health Net). RESULTS: In 
general, adherence to NAEP guidelines was poor. 
Seventy-two percent of respondents with severe 
asthma reported having a steroid inhaler, and of 
those, only 54% used it daily. Only 26% of respon- 
dents reported having a peak flowmeter, and of 
those, only 16% u.sed it daily. Age (older), dura- 
tion of asthma ( longer ), increasing current sever- 
ity of disease, and treatment by an asthma spe- 
cialist correlated with daily use of inhaled steroids. 
Ethnicity (African-American and Hispanic) cor- 
related negatively with inhaled steroid use but pos- 
itively with emergency department visits and hos- 
pital admissions for asthma. Increasing age and 
treatment by an asthma specialist were also iden- 
tified as common factors significantly related to 
the daily use of a peak flowmeter and, interest- 
ingly, to overuse of /J-2 agonist metered dose 
inhalers. CONCLUSIONS: Although the NAEP 
guidelines were published 7 years ago. compli- 
ance with the guidelines was low. It was especially 
poor for use of preventive medication and rou- 
tine peak flow measurement. Furthermore, the 
results showed that asthma specialists provided 
more thorough care than did primary care physi- 
cians in treating patients with asthma. Combin- 
ing the results of the regression analyses revealed 
that some of the variation in rates of emergency 
department visits and hospitali7.ations among some 
subpopulations can be explained by the underuse 
of preventive medication. This study serves the 
goal of documenting the quality of care and ser- 
vices currently provided to patients with asthma 
through a large health maintenance organization 
and provides baseline information that can be used 
to design and assess effective population-based 
asthma disease management intervention pro- 
grams. 

A Randomized Clinical Trial Comparing an 
Extended-Use Hygroscopic Condenser Humid- 
ifier with Heated-Water Humidillcation in 
Mechanically Ventilated Patients — Kollef MH, 
Shapiro SD, Boyd V, Silver P, Von Hiu/ B, Tro- 
villion E, Prentice D. Chest 1998:1 \M?i):1^9. 

OBJECTIVE: To determine the safety and cost- 
effectiveness of mechanical ventilation with an 
extended-use hygroscopic condenser humidifier 
(Duration; Nellcor Puritan-BenneU; Fxlen Prairie, 
MN) compared with mechanical ventilation with 
heated-water humidification. DESIGN: Prospec- 
tive randomized clinical trial. SETI'ING: Med- 



ical and surgical ICUs of Barnes-Jewish Hospi- 
tal, St Louis, a university-affiliated teaching hos- 
pital. PATIENTS: Three hundred ten consecutive 
qualified patients undergoing mechanical venti- 
lation. INTERVENTIONS: Patients requiring 
mechanical ventilation were randomly assigned 
to receive humidification w ith either an extended- 
use hygroscopic condenser humidifier (for up to 
the first 7 days of mechanical ventilation) or 
heated-water humidification. MEASUREMENTS: 
Occurrence of ventilator-associated pneumonia, 
endotracheal tube occlusion, duration of mechan- 
ical ventilation, lengths of intensive care and hos- 
pitalization, acquired multiorgan dysfunction, and 
hospital mortality. RESULTS: One hundred sixty- 
three patients were randomly assigned to receive 
humidification with an extended-use hygroscopic 
condenser humidifier, and 147 patients were ran- 
domly assigned to receive heated-water humid- 
ification. The two groups were similar at the time 
of randomization with regard to demographic char- 
acteristics, ICU admission diagnoses, and sever- 
ity of illness. Risk factors for the development of 
ventilator-associated pneumonia were also sim- 
ilar during the study period for both treatment 
groups. Ventilator-associated pneumonia was seen 
in 15 (9.2% ) patients receiving humidification with 
an extended-use hygroscopic condenser humid- 
ifier and in 15 (10.2%) patients receiving heated- 
water humidification (relative risk. 0.90; 95% con- 
fidence interval = 0.46 to 1.78; p = 0.766). No 
statistically significant differences for hospital mor- 
tality, duration of mechanical ventilation, lengths 
of stay in the hospital ICU, or acquired organ sys- 
tem derangements were found between the two 
treatment groups. No episode of endotracheal tube 
occlusion occurred during the study period in either 
treatment group. The total cost of providing humid- 
ification was $2,605 for patients receiving a hygro- 
scopic condenser humidifier compared with $5,625 
for patients receiving heated-water humidifica- 
tion. CONCLUSION: Our findings suggest that 
the initial application of an extended-use hygro- 
scopic condenser humidifier is a safe and more 
cost-effective method of providing humidifica- 
tion to patients requiring mechanical ventilation 
compared with heated-water humidification. 

The Effect of Physiologic and Mechanical Aging 
on the Performance of Peak How meters — Johns 
DP, Side E, Kendrick AH. Williams TJ. Walters 
EH. Chest 1998;113(-^):774. 

PURPOSE: To investigate the effects of physi- 
ologic and mechanical aging on peak fiowmeters. 
MATERIALS & METHODS: Eight each of Mini- 
Wright (MW; Clement Clark; Harlow, UK), Per- 
sonal-Best (PB; Healtli.Scan PnxiucLs; Cedar Grove 
NJ), Vilalograph (V; Vitalograph Ltd; Buck- 
ingham, UK), and Breath-Taker (BT; Medical 
Development Australia; Melbourne, Australia) 
peak llowmelers were assessed for accuracy and 
repeatability before and after aging using a com- 
puter-driven syringe to deliver peak flows from 



1 00 to 700 L/min. Four of each type of flowme- 
ter were physiologically aged by normal subjects 
performing up to 6 peak flows daily for 1 year. 
The remaining 4 of each flowmeter were mechan- 
ically aged using an accelerated aging device to 
deliver 2,000 exponential waveforms with a peak 
flow of 600 L/min over a period of 3 h. RESULTS: 
The V and BT flowmeters were linear and accu- 
rate over the range 100 to 700 L/min, while the 
PB overread at high flows. The MW was alinear 
throughout. The SD of the difference between 
readings before and after aging ranged from 8.6 
to 40.6 L/min (mean, 9.2). Comparing the slopes 
of the relationship of actual against reference peak 
expiratory flow (PEE) showed that 16 flowme- 
ters— 5 BTs, 6 MWs, 4 PBs, and I V had no sig- 
nificant change in slope afier aging. Mechanical 
aging caused a consistent underreading in PEE at 
high flow rates. Physiologic aging showed a more 
variable pattern both within and between flowme- 
ter types. The MW was the most aft'ected by phys- 
iologic aging, producing overestimates of PEE by 
as much as 100 L/min at 500 L/min. CON- 
CLUSIONS: We conclude that the effects of phys- 
iologic and mechanical aging are different, and 
that while mechanical aging may provide a guide 
to the effects of aging, studies using physiologic 
aging would be more appropriate. 

Patterns of Dissimilarities among Instrument 
Models in Measuring Po,, Pco:- 3"d pH in 
Blood Gas Laboratories — Hansen JE, Casaburi 
R. Chest 1998:1 13(3):780. 

OBJECTIVES: To ascertain the degree of di.s- 
similarilies among blood gas and pH analyzer 
models of the same and different manufacturers 
in measurement of Po;, Pco;, and pH using flu- 
orocarbon containing emulsion (FCE) proficiency 
testing material. DESIGN; Statistically and graph- 
ically analyze data from 6 recent proficiency test- 
ing surveys for the 20 more frequently used mod- 
els of analyzers. SETTING & PARTICIPANTS: 
Over a 2-year period, approximately 900 par- 
ticipants from blood gas laboratories in the United 
States analyzed similar ampules from each of 30 
lots. MEASUREMENTS & RESULTS: Both 
graphic and statistical comparisons were used to 
demonstrate differences between manufacturers. 
For each of the 4 major manufacturers, compar- 
isons revealed statistically significant differences 
not only for Po;, but also for Pco; iind pH. Addi- 
tionally, comparison models within each of the 
3 manufacturers (those with multiple models and 
> 15 insmjments/mtxJel represented) disclosed sta- 
tistically significant dissimilarities among mod- 
els for each analyte in 1 15 of 153 model pairings. 
Previously reported tonometered blixxl difterences 
among analyzer models for Po, are qualitatively 
similai' to the difl'enences found in these same mod- 
els in this FCE smdy. M(xlel differences arc impor- 
tant in research studies and may be clinically 
important in deciding abnormidity. selecting oxy- 
gen therapy, or the treatment of patients with res- 



528 



RESPIRATORY CARE • .IlJI.Y 1998 VOL 4.^ NO 7 



Abstracts 




American Association for Respiratory Care • 1 1030 Abies Ln., Dallas, TX 75229-4593 • (972) 243-2272 • Fax (972) 484-6010 

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Phces subject to change without notice. 



piratory failure or severe respiratory alkalosis. 
CONCLUSIONS: To minimize the likelihood of 
misleading clinicians, laboratory directors should 
consider the degree of dissimilarity among blood 
gas analyzer models in current use and when 
changing instrumentation. 

Rehabilitation of Hypoxemic Patients witii 
COPD at Low Altitude at tlie Dead Sea, the 
Lowest Place on Earth — Kramer MR, Springer 
C. Berkman N, Glazer M, Bublil M, Bar-Yishay 
E, Godfrey S. Chest 1998;1 13(.1):571. 

BACKGROUND: In patients with COPD, oxy- 
gen therapy has been shown to improve exercise 
capacity and survival. Increase in barometric pres- 
sure at low altitude can serve as a simple way to 
improve arterial oxygenation in hypoxemic 
patients. We have tried to evaluate the effect of 
staying at low altitude on arterial oxygenation and 
exercise performance in patients with COPD. 
PATIENTS & METHOD: Eleven patients with 
COPD (9 male, 2 female) aged 38 to 79 years 
(mean f^V|. 0.96 L: 36% predicted) with hypox- 
emia (mean PaO:- 54.2 ± 8.9 mm Hg) at Jerusalem 
(altiuide 8(X) m above sea level) were taken down 
to the Dead Sea area (altitude 402 m below sea 
level! for 3 weeks. At both locations we tested 
arterial blood gases, spirometry, progressive exer- 
cise. 6-min walking distance, and sleep oxime- 



try. The study was repeated 2 weeks after return- 
ing to Jerusalem. RESULTS: Spirometry results 
were unchanged. Mean arterial P^o; rose from 
54.2 ± 8.9 mm Hg to 69.5 ± 1 1 at the first week 
and to 66.6 ± 1 1 at the third week of stay (p < 
0.(.)01 ). Pacoi ro.se from 43.5 ± 9.8 mm Hg to 47.7 
± 9 and 49.5 ± 8.4 (p < 0.006). Six-min walking 
distance rose from 337 ± 107 m to 449 ± 73 and 
507 + 91 in the third week (p < 0.005). Maximum 
oxygen consumption (Vo:max) rose from 901 ± 
257 niL/min to 1,099 ± 255 and 1,063 ± 250 
mL/min (p = 0.01 ). Sleep oximetry showed an 
increase in mean sleep arterial oxygen sahiration 
from 86.0 ± 4.3% to 89.9 ± 4.2% and 88.3 ± 3.0 
at 1 and 3 weeks, respectively (p < 0.05). Fol- 
lowing the return to Jerusalem, arterial gases 
returned to their baseline levels (PaO:. 52.9 ± 9.4 
mm Hg) but 6-min walking distance remained 
significantly high, 453 ± 47 (p < 0.02). and Vojiiiax 
remained high as well (1.102 + 357 mL/min). 
although it did not reach statistical significance. 
CONCLUSIONS: Decline to low altitude or 
staving at high oxygen environment improves 
arterial oxygenation and exercise capacity in 
hypoxemic patients residing in moderate or high 
altitude. Low altitude (or pressurized wards) can 
improve pulmonary rehabilitation of hypoxemic 
patients with COPD. See the related article: What 
Happens in the Dead Sea? (editorial) — Mink VD. 
Chest l99S:II3(3):566-567. 



Validation of a New Dyspnea Measure: The 
UCSD Shortness of Breath Questionnaire. Uni- 
versity of California, San Diego — Eakin EG, 
Resnikoff PM, Prewitt LM. Ries AL, Kaplan RM. 
Chest 1998:113(31:619. 

OBJECTIVE: Evaluate the reliability and valid- 
ity of a new version of the University of California, 
San Diego Shortness of Breath Questionnaire 
(SOBQ), a 24-item measure that assesses self- 
reported shortness of breath while performing a 
variety of activities of daily living. DESIGN: 
Patients enrolled in a pulmonary rehabilitation pro- 
gram were asked to complete the SOBQ, the Qual- 
ity of Well-Being Scale, the Center for Epi- 
demiologic Studies Depression Scale, and a 6-min 
walk with modified Borg scale ratings of perceived 
breathlessness following the walk. SETTING: Uni- 
versity medical center pulmonary rehabilitation 
program. Patients: Thirty-two male subjects and 
22 female subjects with a variety of pulmonary 
diagnoses: COPD (n = 28), cystic fibrosis (n = 9). 
and postlung transplant (n = 17). MEASURE- 
MENTS & RESULTS: The current version of the 
SOBQ was compared with the previous version, 
the fonnat of which often resulted in a significant 
number of "not applicable" answers. The results 
demonstrated that the SOBQ had excellent inter- 
nal consistency (a = 0.96). The SOBQ was also 
significantly correlated with all validity criteria. 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



529 



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Abstracts 



CONCLUSIONS: The SOBQ is a valuable assess- 
ment tool in both clinical practice and research 
in patients w ilh moderate-to-severe lung disease. 

Evaluation of Dyspnea during Physical and 
Speech Activities in Patients with Pulmonary 
Diseases — Lee L, Friescn M, Lambert IR, Loudon 
RG. Chest 1998;113(3):625. 

OBJECTIVES: Dyspnea is most commonly 
assessed by questioning patients about their sub- 
jective perception of shortness of breath during 
physical exertion. Although speech production is 
altered by pulmonary disease, it has not been 
included in current dyspnea assessment tools. 
A questionnaire was developed to address reports 
of dyspnea during ( 1 ) physical activity, (2) speech 
activity, and (3) simultaneous speech and phys- 
ical activity. DESIGN: An equal number of self- 
and experimenter-administered 30-item ques- 
tionnaires was given to 203 patients with restric- 
tive and obstructive pulmonary diseases. Their 
responses were analyzed statistically. RESULTS: 
The questionnaire had high internal consistency 
for individual items within each of the 3 sections. 
The sections were highly correlated but provided 
separate and distinct information. Factors extracted 
from each section were related to severity of dys- 
pnea. Pairwise ; tests demonstrated highly sig- 
nificant differences in subject responses to the 
3 sections. The least dyspnea was experienced 
during speech activities, more during physical 
activities, and the most when speech and phys- 
ical activities were combined. CONCLUSIONS: 
The questionnaire proved to be a quickly admin- 
istered tool for providing information about the 
effect of dyspnea on activities of daily living. 
Because of the emphasis on dyspnea during 
speech production, it may be particularly useful 
for assessing patients who rely extensively on 
speaking ability for their livelihood. 

Rate of FEV] Change following Lung Volume 
Reduction Surgery — Brenner M, McKenna RJ 
Jr. Gelb AF. Fischel RJ, Wilson AF. Chest 
1998;I13(3):652. 

INTRODUCTION: Lung volume reduction 
surgery (LVRS) improves pulmonary function 
and dyspnea symptoms acutely in selected patients 
with heterogeneous emphysema. Limited data are 
available regarding long-term function follow- 
ing LVRS. We analyzed short-tenn (< 6 months) 
and long-temi rate of change of pulmonary func- 
tion in 376 patients who underwent unilateral or 
bilateral LVRS using thoracoscopic or median 
stemotoiny, staple, laser, or combined techniques. 
We hypothesized that the long-term rate of dete- 
rioration in lung function would be dependent on 
the surgical procedure used and would be great- 
est in those with the largest short-term postop- 
erative improvement. MHTIIODS: Pulmonary 
function was assessed preoperalively and at 
repeated intervals following LVRS. The change 



in pulmonary function over time was assessed for 
each patient by determining the individual change 
in FEV I using linear regression analysis short and 
long term. Overall rate of change in pulmonary 
function was calculated for the composite group 
of patients and subgrouped by operative proce- 
dure. RESULTS: Lung function appears to 
improve in the first few months following LVRS 
in most patients, maximizing at approximately 

3 to 6 months and declining thereafter. The short- 
term incremental improvement following staple 
procedures is superior to improvements following 
laser procedures or unilateral surgery: FEV| 
increase (mean ± SD) of 0.39 + 0.03 L for bilat- 
eral staple, 0.25 ± 0.03 L for unilateral staple, 0. 10 
± 0.03 L for unilateral laser, and 0.22 ± 0. 1 L for 
mixed unilateral staple/laser procedures. How- 
ever, the long-term rate of decline in FEV| was 
greatest for bilateral staple LVRS procedures as 
well: 0.255 + 0.057 L/y for bilateral staple, 0. 1 07 
± 0.068 L/y for unilateral staple, 0.074 + 0.034 
L/y for unilateral laser, and 0.209 ± 0. 1 2 L/y for 
mixed staple laser procedures. There was a gen- 
eral correlation between the magnitude of short- 
term incremental improvement and the rate of 
deterioration in FEVi (r = 0.292, p = 0.003). 
CONCLUSIONS: While bilateral staple LVRS 
procedures lead to greater short-term improve- 
ment in FEV i , the more rapid rate of FEV i decl i ne 
in these patients and the general association 
between greater short-tenn incremental improve- 
ment and higher rates of deterioration raise ques- 
tions regarding optimal long-term procedures. Fur- 
ther studies will be needed to answer these 
important questions. 

Transcutaneous Pco2 To Monitor Noninvasive 
Mechanical Ventilation In Adults: Assessment 
of a New Transcutaneous Pco2 Device — 

Janssens JP, Howaith-Frey C, Chevrolet JC, Abajo 
B, Rochat T. Chest 1998:1 13(3):768. 

The present study was designed to analyze the 
usability of a commercially available, transcu- 
taneous Pco; (TcPco: ) sensor for monitoring non- 
invasive positive pressure ventilation (NPPV). 
Twenty-six hemodynamically stable patients with 
intra-arterial radial catheters were assessed. After 
stabilization of TcPco:- arterial blood was ana- 
lyzed and results were compared with TcPco; at 
time of sampling. To evaluate the drift of the sig- 
nal, samples were taken hourly in 5 patients for 

4 h while continuously recording TcPco:- Finally, 
to assess for the response of the sensor to changes 
in Paco;. 6 patients underwent continuous TcPco; 
recording while initiating or interrupting NPPV; 
arterial samples were analyzed before the event, 
and I, 3, 5, 7. 9, and 20 min afterwards. 
RESULTS: TcPcoj and Paco; were tested over 
a range of 26 to 7 1 mm Hg and were found to be 
closely con-elated (r = 0.968, p < 0.0001 ); mean 
bias was 0.75 nmi Hg. There was no significant 
drift of TcPco. as compared with Paco; over4 h. 
Ihe time of response of TcPfo; to initiation or 



interruption of NPPV was < 60 s. An estimation 
of the lag time averaged 5 + 3 min (range, 1 to 9 
min). CONCLUSION: TcPco, in hemodynam- 
ically stable adults was in excellent agreement with 
arterial measurements. The time of response to 
a change in ventilation was compatible with the 
aiin of clinical monitoring of patients under NPPV. 

Patient-Induced Complications of a Heimlich 
Flutter Valve— Crocker HL, Ruffin RE. Chest 
I998;113(3):838. 

Heimlich flutter valves have gained widespread 
acceptance in the treatment of pneumothorax. 
However, some features of their design may pre- 
dispose them to inadvertent misuse. A case of ten- 
sion pneumothorax is described which resulted 
from the insertion of a drinking straw into the 
Heimlich flutter valve a.ssembly. 

Use of Conventional and Self-Adjusting Na.sal 
Continuous Positive Airway Pressure for Treat- 
ment of Severe Obstructive Sleep Apnea Syn- 
drome: A Comparative Study — Konemiann M, 
Sanner BM. Vyleta M, Laschewski F, Groetz J, 
Sturm A, Zidek W. Chest 1998;1 13(31:714. 

OBJECTIVES: To compare conventional and self- 
adjusting nasal continuous positive airway pres- 
sure (nCPAP) therapy in patients with severe 
obstructive sleep apnea syndrome with respect to 
suppression of respiratory disturbances, quality 
of sleep, mean mask pressure, and patient com- 
pliance. DESIGN: Cohort study of consecutive 
patients with obstructive sleep apnea syndrome, 
single-blinded. SETTING: Clinical sleep labo- 
ratory in Gennany. PATIENTS: Fifty patients (44 
men, 6 women who ranged in age from 35 to 7 1 
years) with polysomnographically confirmed 
severe obstructive sleep apnea syndrome (res- 
piratory disturbance index [RDI], > 20/h). MEA- 
SUREMENTS & INTERVENTIONS: After base- 
line polysomnography, patients were randomly 
treated with nCPAP either in conventional (Group 
1 ) or in automatically adjusting (Group 2) mode. 
Three to 6 months after adjustment, all patients 
underwent polysomnography again. They also 
were exainined with a portable monitoring device 
and received a questionnaire on subjective well- 
being and device evaluation. RESULTS: Anthro- 
pometric and respiratory data were comparable 
in both groups; body mass index had not changed 
significantly in the follow-up. RDI dropped by 
9 1 .5% ( from 38.3 ± 1 3.9/h to 3.6 ± 4.4/h ) in con- 
ventional and by 93.67r (from 35.5 ± 9.6/li to 2.4 
± 1 .6/h) in .self-adjusting mode (statistically not 
significant [NS]). Sleep efficiency decreased by 
4.0% in conventional and increased by 2.0% in 
self-adjusting mode (NS). In botli groups, normal 
sleep structure was largely restored. Mean mask 
pressure was 8. 1 ± 2.5 cm H;0 in Group 1 and 
6.5 ± 1 .7 cm H;0 in Group 2 (p < 0.0 1 ). Patient 
compliance in terms of nights per week of mask 
appliance was better in the self-adjusting mode 



532 



RnspiR.ATORY Care • July 1 W8 vol 43 No 7 



Abstracts 



(5.7 ± 0.7 to 6.5 ± 0.4; p < 0.01). CONCLUSION: 
Self-adjusting nCPAP demonstrates the sanie reli- 
ability in suppression of respiratory disturbances 
as fixed-mask pressure therapy. Sleep quality is 
slightly superior, patient compliance is highly sig- 
nificantly better. 

Hour-to-Hour Variability of Oxygen Satura- 
tion in Sleep Apnea — Chaudhiin B. Dasti S. Park 
Y, Brown T. Davis H. Akhtar B. Chest 
1998;113(3):719. 

OBJECTIVES: Methods used to express the sever- 
ity of oxygen desaturation during polysomno- 
graphy include the average oxygen saturation 
( AOi). lowest oxygen saturation (LO:), and the 
percent of the total time with oxygen saturation 
level lower than 90% (t < 90%). We wanted to 
determine which one of these methods is least 
variable during different hours of monitoring. 
DESIGN: Prospective, observational study. SET- 
TING: Sleep center at a medical university. 
PATIENTS: One hundred fifty patients with 
apnea-hypopnea index from 5 to 130. MEA- 
SUREMENTS: AO2. LO2, and t < 90% were cal- 
culated during each of the 8 h of polysomnog- 
raphy. Data for each hour were compared and the 



Cmnbach a coefficients were calculated. RESULTS: 
There was a high degree of correlation ainong the 
three methods as well as between each method 
and the severity of sleep apnea. The mean ± SD 
values for each method were as follows: AO2. 
92.7 ± 5.6: LO2, 68.5 ± 19.3: and t < 90%, 15.7 
± 24.2. The a coefficients for these methods were 
AO2, 0.98; LO2. 0.88; and t < 90%, 0.98. In all 
methods, the data of the first hour were signifi- 
cantly different from the data of the subsequent 
hours. CONCLUSION: Both AO2 and t < 90% 
methods show less hour-to-hour variability com- 
pared with LO2, and there is more variability in 
the first hour. Since the AO2 values > 90% may 
not convey the severity of O2 desaturation, t < 90% 
may be the best method of expressing oxygen sat- 
uration changes during polysomnography. 

The Effect of a Mandibular Advancement 
Device on Apneas and Sleep in Patients with 
Obstructive Sleep Apnea — Marklund M, 
Franklin KA. Sahlin C, Lundgren R. Chest 
1998:113(31:707. 

OBJECTIVE: To evaluate the effects of a mandibu- 
lar advancement device on apneas and sleep in 
mild, moderate, and severe obstructive sleep 



apnea. DESIGN: Prospective study. SUBJECTS: 
Forty-four of 47 parients included. INTER- 
VENTION: Individually adjusted mandibular 
advancement devices. MEASUREMENTS: 
Polysomnographic sleep recordings for I night 
without the device and 1 night with it, with a 
median of 1 day and no changes in weight, med- 
ication, or sleep position between the recordings. 
RESULTS: The device reduced the median 
obstructive apnea-hypopnea index from 1 1 (range, 
7 to 19) to 5 (range, to 17) (p < 0.001) in 21 
patients with mild sleep apnea, from 27 (range, 
20 to 38) to 7 (range, 1 to 19) (p < 0.001) in 15 
patients with moderate sleep apnea, and from 53 
(range, 44 to 66) to 14 (range, 2 to 32) (p < 0.05) 
in 8 patients with severe sleep apnea. The arousal 
index decreased and the sleep stage patterns 
improved in all severity groups. Twenty-eight of 
44 patients were successfully treated with an 
obstructive apnea-hypopnea index of below 10 
and a subjective reduction in snoring. Nine of 16 
patients with treatment failure still reported a reduc- 
tion in snoring. The success rate correlated 
inversely to the disease severity (r = -0.41; p < 
0.01 ). CONCLUSIONS: A mandibular advance- 
ment device reduces apneas and improves sleep 
quality in patients with obstructive sleep apnea. 



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RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



533 



Abstracts 




1998 

LITERARY 

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especially in those with mild and moderate dis- 
ease. A follow-up sleep recording during treat- 
ment is necessary because of the risk of silent 
obstructive apneas without subjective snoring with 
the device. 

Determinants of EfTective Ventilation during 
Nasal Intermittent Positive Pressure Venti- 
lation — Parreira VF. Jounieaux V, Delguste P. 
Aubert G. Dury M. Rodenstein DO. Eur Respir 
J 1997:10(9):1975. 

Our aim was to verily in healthy subjects submitted 
to nasal intermittent positive pressure ventilation 
(nIPPV ) with a volumetric ventilator on controlled 
mode, whether changes in ventilator settings 
(delivered tidal volume (Vf), respiratory frequency 
(f) and inspiratory flow (V|) could influence 
effective minute ventilation (Vp). thus allow- 
ing identification of the settings resulting in the 
highest V). during nIPPV. We then compared 
these experimentally obtained "best" settings to 
those obtained retrospectively in a group of 
patients submitted to long-term nlPPV for clin- 
ical reasons. We studied 10 healthy subjects awake 
and asleep, and .^.^ patients with restrictive ven- 
tilatory disorders. Changes in delivered V| (lor 
a constant delivered Vt and f") led to significanl 
changes in Vi.;. Vj.was significantly higher when 
a given delivered Vk was obtained using higher 



f and lower Vx than when it was obtained using 
lower delivered f and higher Vj. Increases in f gen- 
erally resulted in increases in Vg. The "best" set- 
tings derived from these results were: Vj. 1 3 mL 
kg ' of body weight; f: 20 breaths/min' and Vi: 
0.56-0.85 L s '.The corresponding average val- 
ues found in the patient group were: delivered Vy: 
14 niL ■ kg"'; f: 23 breaths/min ' and delivered 
V|: 0.51 L s"'. Changes in minute ventilation 
resulting from modifications in ventilator settings 
can be attributed to the glottic response to mechan- 
ical influences. This leads to "ideal" settings quite 
different from the standard ones in incubated 
patients. Values derived from nasal intermittent 
positive pressure ventilation in healthy subjects 
seem to apply to patients submitted to long-term 
nasal intermittent positive pressure ventilation. 

Lung Deposition from the Turbuhaler in Chil- 
dren with Cystic Fibrosis — Devadason SG. Ever- 
ard ML, MacF.arlan C. Roller C. Summers QA, 
Switl P, el al. Eur Respir J 1997;IO(9):2023. 

Drug delivery to patients using dry powder 
inhalers, such as the Turbuhaler. is believed to be 
inlluenced by the inspiratory fiow used. Clinical 
studies have indicated that this delivery .system 
caEi be used effectively by children. However, it 
is not known how the total and weight-corrected 
dose delivered to the airways varies with age. A 



deposition study using lechnetium-99m (99mTc)- 
labeled budesonide was performed in order to 
determine the effect of age on delivery. Twenty 
one children with cystic fibrosis, aged 4- 1 6 y, were 
recruited. They were clinically stable with nor- 
mal lung function. Initially, a ycaniera scan was 
taken in front of a flood source containing 37 MBq 
of 99mTc. Subsequently, subjects inhaled through 
a low resistance inspiratory filter connected to a 
commercially available Turbuhaler. Immediately 
afterwards they inhaled from a noncommercial 
Turbuhaler containing budesonide labeled with 
99mTc, and then underwent anterior and poste- 
rior y camera scans. Botli Turbuhaler inhalers were 
attached to a portable spirometer and the peak 
inspiratory flow through the Turbuhaler was 
recorded for each inhalation. The total body dose 
was calculated from the dose deposited on the 
inspiratory filter connected to the commercial Tur- 
buhaler. Analysis of the ycamera images provided 
information on the proportion of the radiolabel 
delivered to the lungs compared to that deposited 
in the upper airway and stomach. As expected, 
a highly significant positive correlation was noted 
between the peak inspiratory flow generated by 
the patient through the Turbuhaler and the dose 
delivered to the lung. Similaily, there was a highly 
significant positive correlation between age and 
"total lung dose." However, when total lung dose 
was conected for body weight, there was a non- 



534 



Respiratory Care 'Jlily 1998 Vol 43 No 7 



Abstracts 



significant negative coirelation with age. This study 
suggests that the "weight-corrected lung dose" 
achieved when children aged > b yrs use the Tur- 
buhaler. Is largely independent of age. It would 
appear that the How-dependent properties of this 
device are such that the reduced peak uispiratory 
flow generated by younger children results in a 
lower dose to the lungs, but that this is off-set by 
their lower body weight. This is unlikely to be a 
property of other devices with different flow/dnig 
delivery characteristics. 

The Effect of Lov^-Uosc Inhalation of Nitric 
Oxide in Patients with Pulmonary Fibrosis — 

Yoshida M. Taguchi O, Gabazza EC, Yasui H. 
Kobayashi T. Kobayashl H. et al. Eur Respir J 
19y7;10(9):205l. 

The aim of this study was to determine w hether 
low-dose inhalation of nitric oxide (NO) improves 
pulmonary haemodynamics and gas exchange in 
patients with stable idiopathic pulmonary fibro- 
sis (IPF). The investigation included 10 IFF 
patients breatliing spontaneously. Haemodynaiiiic 
and blood gas parameters were measured under 
the following conditions: ( 1 ) breathing room air; 
(2) during inhalation of 2 parts per million (ppm) 
NO with room air: (3) whilst breathing O; alone 
(1 L min 'l: and (4) dunng combined inhalation 
of 2 ppm NO and O: ( 1 L ■ min'). Dunng inhala- 
tion of 2 ppm NO with room air the mean pul- 
monary arterial pressure (Ppa 25 ± 3 vs 30 ± 4 mm 
Hgl and the pulmonary vascular resistance (PVR 
S2y ± 80 vs 699 ± 1 10 dyn • s ■ cm*) were sig- 
nificantly (p < 0.01 ) lower than levels measured 
whilst breathing room air alone. However the arte- 
rial oxygen tension (Pao.-) did not improve. The 
combined inhalation of NO and Oi produced not 
only a significant (p < 0.01 ) decrease of Ppa (23 
± 2 vs 28 ±3 mm Hg) but also, a remarkable 
improvement (p < 0.05) in PjO; ( 14.2 ± 1 .2 vs 1 1 .7 
+ 1 .0 kPa) ( 107 + 9 vs 88 ± 7 mm Hg) as com- 
pared with the values observed during the inhala- 
tion of O; alone. These findings suggest that the 
combined use of nitric oxide and oxygen might 
constitute an alternative therapeutic approach for 
ffeating idiopathic pulmonary fibrosis patients with 
pulmonary hypertension. However, further stud- 
ies must first be carried out to demonstrate the ben- 
eficial effect of oxygen therapy on pulmonary 
haemodynamics and prognosis in patients with 
idiopathic pulmonary fibrosis and to rule out the 
potential toxicity ol inhaled nitric oxide, partic- 
ularly when used in combination with oxygen. 

Use of Conventional and Self-Adjusting Nasal 
Continuous Positive Airway Pressure for Treat- 
ment of Severe Obstructive Sleep Apnea Syn- 
drome: A Comparative Study — Konermann M. 
Sanner BM. Vyleta M, Laschewski F, Groetz J. 
Sturm A, Zidck W. Chest 1998:1 13(3);7I4. 

OBJECTIVES: To compare conventional and 
self-adjusting nasal conUnuous positive airway 



pressure (nCPAP) therapy in patients with .severe 
obstructive sleep apnea syndrome with respect 
to suppression of respiratory disturbances, qual- 
ity of sleep, mean mask pressure, and patient com- 
pliance. DESIGN: Cohort study of consecutive 
patients with obstructive sleep apnea syndrome, 
single-blinded. SETTING: Clinical sleep labo- 
ratoi7 in Gemiany. PATIENTS: Fifty patients (44 
men, 6 women who ranged in age from 35 to 7 1 
years) with poly.somnographically confirmed 
severe obstructive sleep apnea syndrome (res- 
piratory disturbance index |RDI], > 2()/h). MEA- 
SUREMENTS & INTERVENTIONS: After 
baseline polysomnography, patients were ran- 
domly seated with nCPAP either in conventional 
(Group 1 ) or in automatically adjusting (Group 
2) mode. Three to 6 months after adjustment, all 
patients underwent polysomnography again. They 
also were examined with a portable monitoring 
device and received a questionnaire on subjec- 
tive well-being and device evaluation. RESULTS: 
Anthropometric and respiratory data were com- 
parable in both groups; body mass index had not 
changed significantly in the follow-up. RDI 
dropped by 91.5% (from 38.3 + 13.9/h to 3.6 ± 
4.4/h) in conventional and by 93.6% (from 35.5 
± 9.6/h to 2.4 ± 1 .6/h) in self-adjusting mode (sta- 
tistically not significant |NS1 1. Sleep efficiency 
decreased by 4.0% in conventional and increased 
by 2.0% in self-adjusting mode (NS), In both 
groups, normal sleep structure was largely 
restored. Mean mask pressure was 8. 1 ± 2.5 cm 
H2O in Group 1 and 6.5 + 1.7 cm HiO in Group 
2 (p < 0.01). Patient compliance in terms of 
nights/wk of ma.sk appliance was better in the self- 
adjusfing mode (5.7 ± 0.7 to 6.5 ± 0.4: p < 0.01 ). 
CONCLUSION: Self-adjusting nCPAP demon- 
strates the same reliability in suppression of res- 
piratory disturbances as fixed-mask pressure ther- 
apy. Sleep quality is slighlly superior, patient 
compliance is highly significantly better. 

Partial Liquid Ventilation with Small Volumes 
of FC 3280 Increases Survival Time in Exper- 
imental ARDS— Kaisers U, Max M. Walter J, 
Kuhlen R. Pappert D, Falke K, Rossamt R. Eur 
Respir J 1997:10(9): 1955. 

The aim of this study was to determine the pro- 
longed effects of .sequential doses of a highly puri- 
fied peril uorocarbon (FC 3280) on gas exchange 
and survival time in experimental acute respira- 
tory distress syndrome (ARDS). The study was 
prospective, randomized, and controlled. Twelve 
pigs (body weight 30 ± 5 (mean ± SD) kg) were 
surfactant-depleted by repetifive lung lavages, 
reducing arterial oxygen tension (PaO:) to 6.9 ± 
1,6 kPa (52 + 12 mm Hg) (mean ± SD) at an 
inspired oxygen fraction (FioO of 1 .0. They were 
then randomized to receive partial liquid venti- 
lation by sequential intratracheal application of 
7 5 mL kg-i FC 3280 at 30 min intervals to a 
cumulative dose of 15 niL ■ kg"' (treatment group), 
or to receive no further U-eatmenl (conttol group). 



Haemodynamics and gas exchange were assessed 
at 30 min intervals afier instillation, and hourly 
afterwiyds in both groups until death. In the treat- 
ment group. Pal); was 8.9 ± 4.4 kPa (67 ± 33 mm 
Hg) after 7.5 mL kg ' FC 3280 and 14.1 +9.9 
kPa ( 1 06 ± 74 mm Hg) after 1 5 mL ■ kg ' FC 3280 
(NS). In the conU"ol group, gas exchange remained 
unchanged. Haemodynamics were stable in the 
treatment group and deteriorated in the control 
group. Peak airway pressures and dynamic com- 
pliance were not significantly affected in the treat- 
ment group. Mean survival time was 8.2 ± 4.5 h 
in the U'eatment group and 1 .8 ± 1 .4 h in the con- 
trol group (p < 0.05). Upon histological exami- 
nation, both stud) groups were not significantly 
different in tolal lung injury scores. We conclude 
that partial liquid ventilation with small volumes 
of FC 3280 provides improvement in gas exchange 
and increases survival time in experimental acute 
respiratory distress syndrome. See the reluled 
urticle: Partial Liquid Ventilation (editorial) — 
Veihruage SJ. Uuhmann B. Eur Respir J 1 997: 
I0{9}:I9.U-I9}9. 

Autoset Nasal CPAP Titration: Constancy of 
Pressure, Compliance and F^ffectiveness at 8 
Month Follow-Up — Teschler H. Farhat AA, 
Exncr V. Konietzko N. Berthon-Jones M. Eur 
Respir J 1997;10(9):2073. 

We have previously shown that AutoSet satis- 
factorily improves sleep-disordered breathing and 
sleep architecture in subjects with obstructive sleep 
apnoea(OSA) syndrome. The ami of this study 
was to determine, in subjects treated with long- 
tenii conventional fixed pressure continuous pos- 
itive airway pressure (CPAP) at the AutoSet rec- 
ommended pressure, whether: the long-term 
compliance is satisfactory: the improvement per- 
sists once initial rebound is over: the titration pres- 
sure IS stable with time: and the titration pressure 
IS comparable with manual titfation pressure using 
a similar end point. Twenty males with OSA. pre- 
viously studied with full polysomnography on their 
diagnostic night, at manual and AutoSet tiU'ation. 
and at the AutoSet recommended fixed pressure, 
were re-studied after a mean of 3 and 8 months 
of treatment at the recommended fixed pressure. 
Re-study included home respiratory monitoring 
(Nellcor EdeiiTrace). and repeated manual and 
AutoSet titration with polysomnography. Com- 
pliance was as.sessed with hour-meter readings. 
Mean (±SEM) usage was 5.7 ±0.1 h/night ' at 
3 and 8 months. The arousal index remained nor- 
malized. Diagnostic respiratory disturbance index 
(RDI) was 60.3 ± 5.7 events/h ', On AutoSet at 
fi.xed CPAP. RDI was initially 2.6 ± 0.7 ev ents/h ' . 
then rose slightly (p < 0.00 1 ) to 4.3 ± 0.6 evenk/h ' 
at 3 months, and was 3.6 ± 0.5 events/h"' at 8 
months. AutoSet tiU^ation pressure was: 9.9 ± 0.4 
cm H2O initially, 10.6 ± 0.4 cm H^O at 3 months, 
and 9.7 ± 0.5 cm H;0 at 8 months (NS). Manual 
titration pressure at 8 months was 10.4 ± 0.4 cm 
HiO. The standard deviation of the discrepancy 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



535 



ABSTRACTS 



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with AuloSet was 0.84 cm H2O. In conclusion, 
the AutoSet recommended pressure varies little 
with time, and closely predicts the final manual 
titration pressure; the improvement in respirator)' 
disturbance index was largely maintained, and 
compliance was good, although probably enhanced 
by close supervision. 

VValer Vapour and Carbon Dioxide Decrea.se 
Nitric Oxide Keading.s — van dcr Mark TW. Kort 
E, Meijer RJ, Postma DS, KoeterGH. Eur Respir 
J l')97;10(9):2120. 

Mea.surement of nitric oxide levels in exhaled air 
is commonly performed using a chemilumines- 
cence detector. However, water vapour and car- 
bon dioxide affect the chemiluminescence pro- 
cess. The influence of these gases at the 
concentrations present in exhaled air, has not yei 
been studied. For this in vitro study, inixtures of 
.iO. I(X), and 200 parts per billion (ppbl NO in air 
were prepared and fed into the NO analyser cither 
directly or bubbled through water. Mixtures with 
COj were prepared by adding 0- 1 0% CO: !>' 'he 



diluent air. We found a significant decrease in NO 
readings in the water-saturated samples compared 
to the dry gas (p < 0.001). strongly dependent on 
the partial pressure of water. NO levels in exhaled 
air (mean 10 ± 2 ppb) showed a decrease of 17 
± y/c when water vapour was not absorbed. From 
the experiments with CO1 we found a decrease 
in NO reading of l.()4 + 0.07%/volumeCO2(%). 
Presence of water vapour, thus, leads to a sys- 
tematic underestimation of NO levels. Insertion 
of a water absorber might, therefore, be advan- 
tageous. The influence of CO2 concentrations in 
the normal respiratory range is negligible. With 
high expiratory CO: levels as applied in permissive 
hypercapnia, the effects may be substantial. 

Airway Deposition and Airway Effects of Anti- 
asthnia Drugs Delivered from Metered-Dose 
Inhalers — Pauwels R. Newman S. Borgstrom L. 
Eur Respir .1 1W7;10(4):2127. 

Many different metered dose inhalation devices 
are becoming available for the treatment of air- 
wav diseases. Each of these inhalers differs in its 



delivery characteristics. An assessment of the effi- 
cacy of drug delivery by these inhalers is essen- 
tial, in view of their therapeutic use. A review of 
the literature on the relationship between airway 
deposition and airway effects of drugs delivered 
from inetered dose inhalers is presented. Nebu- 
lizers or spacers are not discussed. The effect of 
an inhaler depends on the characteristics of the 
inhaler and the inhalation manoeuvre performed 
by the patient. This review focuses on the influ- 
ence of inhaler characteristics on the airway depo- 
sition and airway effects. Data from several stud- 
ies show that there is a significant relationship 
between the amount of dnig deposited in the air- 
ways and the airway effects of the drag. .Studies 
on the relationship between airway deposition and 
airway effect have been troubled by method- 
ological problems, such as the absence of mul- 
tiple dose comparisons and the difficulty in obtain- 
ing steep dose-response curves. The techniques 
for measuring airway deposition of inhaled drugs, 
namely the scintigraphic and the ph;umacokinetic 
methixi, are discussed and compared. The appro- 
priate use ofthese techniques can help to dellne 



536 



RF.SPIRATORY CARH • JULY 1 W8 VOL 43 NO 7 



ABSTRACTS 



and c"ompare the drug delivery characteristics of 
different devices, thus enabling inhaled therapy 
to be optimized. 

Intensive Care 1980-1995: Change in Patient 
Characteristics, Nursing Workload and Out- 
come — Jakob SM. Rothen HU. Intensive Care 
Med I997;23(II):II65. 

OBJECTIVE: To assess temporal changes in 
patient characteristics, nursing workload and out- 
come of the patients and to compare the actual 
amount of available nursing staff with the esti- 
mated needs in a medical-surgical intensive care 
unit (ICU). DESIGN: Retrospective analysis of 
prospectively collected data. SETTING: A med- 
ical-surgical adult ICU in a Swiss university hos- 
pital. PATIENTS: Data of all patients staying in 
the ICU between January 1980 and December 
1995 were included. INTERVENTIONS: None. 
MEASUREMENTS & RESULTS: The estimated 
number of nurses needed was defined accord- 
ing to the Swiss Society of Intensive Care 
Medicine (SGI)grading system: CalegO[yI=lnurse/ 
patient/shift (= 8 h). Category II = 1 nurse/2 
patients/shift. Category EI = 1 nurse/3 patients/ 
shift. An intervention score (IS) was obtained, 
based on a number of specific activities in the ICU. 



There was a total of 35.327 patients (32% med- 
ical and 68% postoperative/trauma patients). Over 
time, the number of patients/year increased 
(1980/1995: 1,825/2,305, p < O.OOI ) and the length 
of ICU stay (LOS) decreased (4. 1/3.8 days, p < 
0.013). There was an increase in the number of 
patients aged > 70 years ( 19%/28%. p < 0.001 ), 
and a decrease in the number of patients < 60 years 
(58%/4l%, p < 0.001). During the same time 
period, the IS increased 2-fold. Measurement of 
nursing workload showed an increase over time. 
The number of nursing days/year increased 
(1980/1995: 7454/8681, p < 0.019). as did the rel- 
ative amount of patients in Category I (49%/7 1%, 
p < 0.(X)1 ), whereas the portion of patients in Cat- 
egory II (4I%/28%, p< 0.019) and Category III 
(10%/0%) decreased. During the same time 
period, mortality at ICU discharge decreased 
(9.0^/7.0%, p < 0.002). CONCLUSIONS: Dur- 
ing the last 16 years, there has been a marked 
increase in workload at this medical-surgical ICU. 
Despite an increase in the number of severely sick 
patients (as detmed by the nursing grading sys- 
tem) and patient age, ICU mortality and LOS 
declined from 1980 to 1995. This may be ascribed 
to improved patient treatment or care. Whether 
an increasingly liberal discharge policy (transfer 
to newly opened intermediate care units, trans- 



fer of patients expected to die to the ward) or a 
more rigorous triage (denying admission to patients 
with a very poor prognosis) are confounding fac- 
tors cannot be answered by this investigation. The 
present data provide support for the tenet that there 
is a trend toward more complex therapies in increas- 
ingly older patients in tertiary care ICUs. Calcu- 
lations for the number or nurses needed in an ICU 
should take into account the increased turnover of 
patients and the changing patient characteristics. 

High Survival Rate in 122 ARDS Patients Man- 
aged .According to a Clinical Algorithm Includ- 
ing Extracorp<ireal Membrane Oxygenation — 

Lewandowski K, Rossaint R. Pappert D. Gerlach 
H. Slama KJ. Weidemann H. et al. Intensive Care 
Med 1997;23(8):819. 

OBJECTIVE: We investigated whether a treat- 
ment according to a clinical algorithm could 
improve the low survival rates in acute respira- 
tory distress syndrome (ARDS I. DESIGN: Uncon- 
trolled prospective trial. SETTING: One university 
hospital intensive care department. PATIENTS 
& PARTICIPANTS: 122 patients with ARDS, 
consecutively admitted to the ICU. INTER- 
VENTIONS: ARDS was treated according to a 
criteria-defined clinical algorithm. The algorithm 




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CRCE THROUGH 
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RESPIRATORY CARE 
AUGUST 1998 



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Mechanical 
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principles and applications 
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Course director: John Marini, MD 
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Richard Branson, RRT 
Alison Froese, MD 
Dean Hess, PhD, RRT 
Nicholas Hill, MD 
Robert Kacmarek, PhD, RRT 



Neil Maclntyre, MD 
Theodore Viarcy, MD 
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RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Circle 110 on reader service card 



537 



Patient 

Assessment 

Course 



CHICAGO, ILLINOIS 

September 11-13, 1998 

To Meet the Demand for the Patient Assessment 
Course, Respiratory Care Practitioners Are Offered 
Another Opportunity to Attend this Landmark Course 

This course has been approved for 12 clock hours for certification 
maintenance purposes by the Commission for Case Manager Certification 



Check-in time will be from noon until 1 :00 PM on Friday afternoon. Following 
the last class, participants will take a 100-item test developed by the NBRC, which 
should take about one and a half hours to complete, and which will be scored on 
site. Attendees should be finished with the test at approximately 1 :00 PM Sunday. 
All activities will be conducted at the Clarion International Quality Inn at O'Hare. 
Space at this course is limited to 200 attendees and preregistration is required. 
Successful completion of the course will earn participants 16 hours of CRCE credit 
and a certificate of course completion. Each attendee will be given a pocket guide 
to physical assessment, which will be helpful on the job. 

AARC Assessment Course/Examination Detailed Content Outline 




1. Obligations of the Respiratory Care Practitioner 
in the Practice of Patient Assessment 

A. Appreciate the cost of care 

B. Understand the scope and limitations of the 
practitioners role in patient assessment 

C. Understand the principle of patient 
self-determination 

D. Appreciate the psychological, social, and physical 
characteristics of wellness/illness 

E. Recognize the patient's right to confidentiality 
R List the principles of informed consent 

► "Eye opener, as far as the health care 
environment, where we are going, and where 
Respiratory needs to be." — Barbara Messier, RRT 
Bossier Medical Center, Bossier City, LA 

2. Perform a Comprehensive Health Assessment 

A. Review patient records 

B. Structure an interview 

C. Conduct an interview 

D. Conduct a physical assessment 

E. Identify needs for referral 

F. Identify patients with potential for high-risk medical 
complications 



G. Accurately document assessment findings 
H. Present findings to a physician 

► "Extremely well done, good tools, great 
resources." — Susan Gill, RRT 
St. Vincent Infirmary, Little Rock, AR 

3. Assess the Caregivers 

A. Identify sites of care and caregivers 

B. Interview the caregivers 

C. Assess the abilities of caregivers to manage 
physical, technological, and emergency situations 

D. Assess home health resources 

4. Assess the Patient's Understanding and 
Compliance with Physician's Orders and Care 
Plan 

A. Review the physician's order with the patient 

B. Assess the patient's understanding of technique and 
components 

► "I gained so many great ideas and educational infor- 
mation! I can hardly wait to get back to my facilities 
and implement them!" — Marcy Graves, RRT 
Harris Methodist Southwest, Ft. Worth, TX 



FLY DELTA 

and pay less than the fares Delta offers to the general 

public. Discounts are available only through 

Delta's toll-free number. 

Call today, or have your travel agent call: 

(800)241-6760 

8:00 am ■ 11;iO pm, Eastern Time, Daily. Refer to File #109967A. 



ALAMO CAR RENTAL 

Alamo is the official car rental company for the AARC 

Assessment Course. Special discount rates are available 

to all AARC attendees. To make your reservation, 

call Alamo's toll-free number: 

(800) 732 3232 

Request Croup ID #72191 . Rate Code GR. Advanced reservation required. 



► "This course gave me the knowledge and direction B. Inspect the patient care environment 

to pursue at our facility." — Gerry Lickliter, RRT C. Determine the resources available to the patient and 

Baptist Health Center, Enid OK family 

D. Document assessment findings 

C. Assess patient ability to administer treatments, use 

equipment, monitor changes, interpret and respond ► "Bravo for a job well done. I plan to share a lot of 
to those changes this information with staff." 

D. Document assessment findings 

6. Assess Continued Appropriateness of Physician 
5. Assess the Patient's Environment as It Relates to Orders and Care Plan 

Health Status and Supporting Physician's Orders A Review physician orders 

A. Identify barriers to wellness B. Evaluate the patient's response to physician orders 

C. Evaluate the appropriateness of the orders and the 

► "Most excellent! I wish my entire staff could have care plan 

attended." — Laurie Bauer, RRT D. Recommend modification of the treatment plan 

St. Joseph Regional Health Center, Hot Springs, AR E. Document assessment findings 

y 

Course Registration Chicago, IL — Registration Deadline August 24, 1998 

* Registration will close on the date noted or when 200 registrations are received. 

First and Last Name 

Title AARC Member # 

Mailing Address (Please indicate which address is shown above: D Work D Home) 



City State Zip 

( ) 



Daytime Phone Specialty 

Advance Registration Required 

D AARC Member $250 U Nonmember $325 

D Check or money order enclosed U Charge my: U MasterCard U VISA 



Credit Card # Expiration Date Signature 

Mail Registration Form 

and checic, payable to AARC: AARC 

11030 Abies Lane 

Dallas, TX 75229-4593 

Phone: (972) 243-2272 

If paying by credit card, you may fax your Registration Form to (972) 484-2720. Cancellations must be made in writing. There will be a 
30% handling fee for cancellations received 21 days before the course begins. No refunds will be made thereafter. 

HOTEL RESERVATIONS 

The Patient Assessment Course will be conducted at the 

Clarion International Quality Inn at O'Hare 

6810 N. Mannheim Road • Rosemont, IL 60018 

Room Rates: $96 single, $96 double, $96 triple, $96 quad, -h12.5% tax 

For reservations call: (847) 297-8464 and identify yourself as an attendee at the 

September 11-13, 1998 AARC Assessment Course • Deadline for Guaranteed Room Rate is August 24, 1998 



Abstracts 



distinguished 2 main treatment groups: The AT- 
sine-ECMO (advanced treatment without extra- 
corporeal membrane oxygenation) groups (n = 73) 
received a meaQnent consisting of a set of advanced 
noninvasi\'e treatment options, the ECMO treat- 
ment group (n = 49) received additional extra- 
corporeal membrane oxygenation (ECMO) using 
heparin-coated systems. MEASUREMENTS & 
RESULTS: The groups differed in both APACHE 
II (16 ±5 vs 18 ±5 points. p = 0.01) and Mur- 
ray scores (3.2 ± 0.3 vs 3.4 ± 0.3 points, p = 
0.0001). the duration of mechanical ventilation 
prior to admission ( 10 ± 9 vs 13 ± 9 days, p = 
0.0151), and length of ICU stay in Berlin (31 ± 
1 7 vs 50 ± 36 days, p = 0.00 16). Initial PaO;/Fio; 
was 86 ± 27 mm Hg in AT-sine-ECMO patients 
that improved to 165 ± 107 mm Hg on ICU day 
1 . while ECMO patients showed an initial P.,oj'F]0: 
of 67 ± 28 mm Hg and improvement to 160 + 102 
mm Hg was not reached until ICU day 1 3. Qsp/Qia 
was significantly higher in the ECMO-treated 
group and exceeded 50% during the first 14 ICU 
days. The overall survival rate in our 122 ARDS 
patients was 75%. Survival rates were 89% in the 
AT-sine-ECMO group and 55% in the ECMO 
treatment group (p = 0.0000). CONCLUSIONS: 
We conclude that patients with ARDS can be suc- 
cessfully treated with the clinical algorithm and 
high survival rates can be achieved. 

Orbital Herniation Associated with Noninvasive 
Positive Pressure Ventilation — Lazowick D. 
Meyer TJ. Pressman M. Peterson D. Chest 
1998;113(3):841. 

A diagnosis of severe obstructive sleep apnea 
was made after a 52-year-old hypertensive man 
developed a large intracranial hemorrhage. Ther- 
apeutic noninvasive positive pressure ventila- 
tion (NPPV) for obstructive sleep apnea and 
hypoventilation was complicated by transient 
unilateral orbital herniation. As best as can be 
determined, this represents a new. potentially 
deleterious side effect of NPPV. 

IPEEP-Induced Tricuspid Regurgitation — 

Artucio H. Hurtado J. Zimet L. de Paula J. Beron 
M. Intensive Care Med I997;23(8):836. 

OBJECTIVE: To determine the presence of tri- 
cuspid regurgitation (TR) in patients affected by 
acute lung injury (ALI) and the adult respiratory 
distress syndrome (ARDS l during mechanical ven- 
tilation with positive cnd-cxpiratory pressure 
(PEEP). DESIGN: A prospective clinical study. 
SETTING: 1 0-bed general intensive care unit in 
'a University Hospital. PATIENTS: 7 consecutive 
patients an age 44.7 ± 8.6 years with a diagno- 
sis of ALI or ARDS were studied. All were on 
mechanical ventilation with PEEP. INTER- 
VI-NTIONS: PEEP was increased in steps of 5 
cm HiO until tlie appearance of TR or up to a limil 
of 20 cm H2O. MEASUREMENTS & RF.SUI .TS: 
Right atrial pressure, pulmonary artery pressure. 



and wedge pressure were measured and cardiac 
output was determined by thermodilution. TR was 
graded from to 3. Standard 2-D echocardio- 
graphic and pulsed-wave images were obtained 
at each level of PEEP. PEEP was increased from 

4 ± 3 to 1 7 ± 2 cm H^O. Mean PAP increased from 
27.7 ± 2.9 to 36.7 ± 3.5 mm Hg (p < 0.02) when 
PEEP was increased. Five patients had compe- 
tent valves and 2 had mild TR at baseline. In 6 
out of the 7. TR either developed or increased 
when PEEP was increased. CONCLUSIONS: Our 
study demonstrated the development of TR after 
the use of PEEP in patients with ALI and ARDS 
as a consequence of pulmonary hypertension and 
right ventricular overloading. Since TR may ran- 
domly affect cardiac output values and derived 
parameters, the assessment of cardiac pert'omiance 
by sonic tcchni(.|ucs such as thermodilution should 
be used with caution. 

Respiratory Comfort of Automatic Tube Com- 
pensation and Inspiratory Pressure Support 
in Conscious Humans — Guttmann J. Bernhard 
H. Mols G, Benzing A. Hofmann P. Haberthiir 
C.etal. Intensive Care Med 1997:23( 1 1 ):1 1 19. 

OBJECTIVE: To compare the new mode of ven- 
tilatory support, which we call automatic tube 
compensation (ATC), with inspiratory pressure 
support (IPS) with respect to perception of res- 
piratory comfort. ATC unloads the resistance of 
the endotracheal tube (ETT) in inspiration by 
increasing the airway pressure, and in expiration 
by decreasing the airway pressure according to 
the nonlinear pressure-flow relationship of the 
ETT. DESIGN: Prospective randomized single 
blind cross-over study. SETTING: Laboratory of 
the Section of Experimental Anaesthesiology 
(Clinic of Anaesthesiology; University of 
Freiburg). SUBJECTS: Ten healthy volunteers. 
INTERVENTIONS: The subjects breathed spon- 
taneously through an ETT of 7.5 mm ID. Three 
different ventilatory modes, each with a PEEP of 

5 cm H:0, were presented in random order using 
the Drager Evita 2 ventilator with prototype soft- 
ware: (1) IPS (10 cm H:0, I s ramp). (2) inspi- 
ratory ATC ( ATC-in). (3) inspiratory and expi- 
ratory ATC (ATC-in-ex). MEASUREMENTS & 
MAIN RESULTS: Immediately following a mode 
transition, the volunteers answered with a hand 
sign to show how they perceived the new mode 
compared with the preceding mode in terms of 
gain or loss in subjective respiratory comfort: "bet- 
ter." "unchanged." or "worse." Inspiration and 
expiration were investigated separately analyz- 
ing 60 mtxie transitions each. Flow rates were con- 
tinuously measured. The transition froin IPS to 
either type of ATC was perceived positively, ic 
as increased comfort, whereas the opposite tran- 
sition from ATC to IPS was perceived negatively, 
ie as decreased comfort. Tlie transition from ATC- 
in to ATC-in-ex was perceived positively whereas 
the opposite mode transition was perceived neg- 
atively in expiration only. Tidal volume was 1220 



± 404 mL during IPS and 1 1 7 + 362 mL during 
ATC. The inspiratory peak flow rate was 959 ± 78 
mL/s during IPS and l(H8 ± 197 mL/s during ATC. 
CONCLUSIONS; ATC provides an increase in 
respiratory comfort compared with IPS. The pre- 
dominant cause for respiratory discomfort in the 
IPS mode seems to be lung over-inflation. 

Interpretation of the Pulmonary Artery Occlu- 
sion Pressure in Mechanically Ventilated 
Patients with Large Respiratory Excursions 
in Intrathoracic Pressure — Hoyt JD. Leather- 
man JW. Intensive Care Med 1997;23( 1 1 ): 1 1 25. 

OBJECTIVE: To assess the reliability of the pul- 
monary artery occlusion pressure (Ppan) when res- 
piratory excursions in intrathoracic pressure are 
prominent. DESIGN: We studied 24 critically 
ill patients who had 15 mm Hg or more of res- 
piratory excursion in their Ppao tracing. Large res- 
piratory excursions resulted from respiratory mus- 
cle activity that persisted despite sedation and 
mechanical ventilation in the assist-control mode. 
From the Ppa„ tracing, the end-expiratory and 
mid-point values were recorded; the latter was 
measured halfway between end-expiration and 
the nadir due to inspiratory triggering. The Ppao 
was then re-measured after administration of a 
non-depolarizing muscle relaxant. SETTING: 
Medical intensive care unit of a university-affil- 
iated teaching hospital. MEASUREMENTS & 
RESULTS; The difference between the prere- 
laxation end-expiratory Ppao and the relaxed Ppao 
was larger than the difference between the pre- 
relaxation mid-point Ppao and the relaxed Ppao 
(11 ±5vs3±3mmHg. p<0.0l). In2l of 24 
(88%) cases, the relaxed Ppa„ was more closely 
approximated by the mid-point Ppa,i than by the 
end-expiratory Ppa„. The difference between the 
end-expiratory Ppao and the relaxed Ppao increased 
as the amount of respiratory excursion increased 
(r = 0.51; p < 0.01). CONCLUSIONS: In 
mechanically ventilated patients whose respi- 
ratory muscles produce large excursions in the 
Ppau. the end-expiratory Ppao is often much higher 
than the Ppa„ measured after muscle relaxation. 
The pre-relaxation mid-point Ppao and the relaxed 
Ppao are usually similar, but this may not be true 
in individual patients. In this setting, the Ppao mea- 
sured after muscle relaxation probably provides 
the most clinically reliable estimate of left heart 
filling pressure. 

Functional Magnetic Stimulation of Expira- 
tory Muscles: .\ Noninvasiv e and New Method 
for Restoring Cough — Lin VWH. Hsieh C. Hsiao 
IN. Canlleld J. J Appl Physiol 1998;84(4): 1 144. 

Tlie purpose of this study was to assess the effec- 
tiveness of functional magnetic stimulation (FMS) 
for producing expiratory function in normal 
human subjects. Twelve able-bodied noniial sub- 
jects were recruited for this study. FMS of the 
expiratory muscles was performed by using a 



540 



RESPIRATORY CARH • Jl'LY 1998 VOL 43 NO 7 



Abstracts 



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magnetic sliinulator and placing tlie magnetic coil 
along the lower thoracic spine. Results showed 
that peak expired pressure, volume, and flow rate 
generated by FMS at the end of normal inspiration 
(102..'i± 13.62 cm H:0. 1.6 + 0.16 L. and 4.8 ± 
0.35 L/s. respectively) were comparable to their 
voluntary maximal levels (p > 0. 1 ). The optimal 
coil placement was between T7 and Til. and the 
optimal stimulation parameters were a frequency 
of 25 Hz and 70-80% of maximal intensity. We 
conclude that ( 1 ) FIVIS of the lower thoracic nerves 
in normal subjects resulted in a significant expi- 
ratory function comparable to their voluntary max- 
imum; (2) FIVIS was noninvasive and was well 
tolerated by all subjects; and (3) FMS may be use- 
ful to produce cough in patients in critical care 
or perioperative settings, or in patients with neu- 
rological disorders. 

Distribution of Inhaled Nitric Oxide during 
Sequential and Continuous AdminLstration into 
the Inspiratory Limb of the Ventilator — Mour- 

geon E. Gallart L, Rao GS, Lu Q. Law-Koune JD. 
Puybasset L, et al. Intensive Care Med 
1997;23(8);849. 

OBJECTIVES: The concentrations of nitric oxide 
(NO) in the ventilatory circuits and the patient's 
airways were compared tietween sequential (SQA) 



and continuous (CTA) administration during inspi- 
ratory limb delivery. DESIGN: Prospective con- 
trolled study. SETTING: Fourteen-bed Surgical 
Intensive Care Unit of a teaching University hos- 
pital. PATIENTS & PARTICIPANTS: Eleven 
patients with acute lung injury on mechanical ven- 
tilation and 2 healthy volunteers. INTERVEN- 
TIONS: A prototype NO delivery device (Opti- 
NO) and Cesar ventilator were set up in order to 
deliver 1. 3. and 6 parts per million (ppm) of NO 
into the bellows of a lung model in SQA and CTA. 
Using identical ventilatory and Opti-NO settings. 
NO was administered to the patients with acute 
lung injury. MEASUREMENTS & RESULTS: 
NO concenu-ations measured from the inspiratory 
limb |lNSP-NOMca^] and the trachea (TRACH- 
NOmcus] using fast response chemiluminescence 
were compared between the lung model and the 
patients using controlled mechanical ventilation 
with a constant inspiratory flow. INSP-NOmjus 
were stable during SQA and tlucUiated widely dur- 
ing CTA (fluctuation at 6 ppm = 61 % in the lung 
model and 58 ± 3% in patients). In patients. 
[TRACH-NOmclsI fluctuated widely during both 
modes (fluctuation at 6 ppm = 55 ± 3% during 
SQA and 54 ± 5% during CTA). The NO flow 
requirement was significantly lower during SQA 
than during CTA (74 ± 0.5 vs 158 ± 2.2 mL/min-' 
to attain 6 ppm, p = 0.000 1 ). INSP-NOmeas were 



close to the values predicted using a classical for- 
mula only during SQA (bias = -0.1 ppm, preci- 
sion = ± 1 ppm during SQA; bias = 2.93 ppm and 
precision = ±3.54 ppm during CTA). During SQA, 
INSP-NOMeas varied widely in healthy volunteers 
on pressure support ventilation. CONCLUSIONS: 
CTA did not provide homogenous mixing of NO 
with the tidal volume and resulted in fluctuating 
INSP-NOmcis- In contrast, SQA delivered stable 
and predictable NO concentrations during con- 
trolled mechanical ventilation with a constant inspi- 
ratory flow and was economical compared to CTA. 
However, SQA did not provide stable and pre- 
dictable NO concentrations during pressure sup- 
port ventilation. 

Predictors of Smoking Cessation after Per- 
cutaneous Coronary Revascularization — Has- 

dai D. Giu-ratt KN, Grill DE, Mathew V, Lemian 
A, Gau GT, Holmes DR Jr. Mayo Clin Proc 
1998;73(3):205. 

OBJECTIVE: To identify factors predictive of 
smoking cessation after successful percutaneous 
coronary revascularization. MATERIAL & 
METHODS: We undertook a case-control study 
of the smoking stanis of all patients at Mayo Clinic 
Rochester from September 1979 through Decem- 
ber 1995 who were smokers at the time of an index 



Respiratory Care • July 1998 vol 43 No 7 



541 



Abstracts 



percutaneous coronary revascularization proce- 
dure in the nonperi-infarction setting (no myocar- 
dial infarction within 24 hours). Maximal dura- 
tion of prospective follow-up was 16 years. Patients 
were classified into those who permanently quit 
smoking immediately after the procedure (n = 435; 
mean follow-up, 5. 1 ± 3.7 years) or those who con- 
tinued to smoke at some time during follow-up 
(n = 734; mean follow-up, 5.3 ± 3.7 years). Logis- 
tics regression models were formulated to deter- 
mine independent predictors of smoking cessa- 
tion. RESULTS: Predictors of continued smoking 
were greater prior cigarette consumption (odds 
ratio [OR] = 1 .009 for each pack-year; 95% con- 
fidence interval [CI] = 1.004 to 1.014)and hav- 
ing one or more risk factors for coronary artery 
disease other than cigarette smoking (OR = 1 .49; 
957r CI = 1.15 to 1.93). Older age (OR = 0.98 for 
each additional year; 95% CI = 0.97 to 0.99) and 
unstable angina at time of initial assessment (OR 
= 0.69; 95%- CI = 0.52 to 0.91 ) were associated 
with less likelihood of continued smoking. CON- 
CLUSION: Younger patients with a worse risk 
profile and greater prior cigarette consumption 
were more likely than other patients to continue 
smoking after percutaneous coronary revascu- 
larization in the nonperi-infarction setting. Patients 
who had unstable angina were more likely lo quit 
smoking than those who had stable angina. Despite 
the proven benefits of smoking cessation after per- 
cutaneous coronary revascularization, a substantial 
proportion of smokers (63%) continue to smoke; 
thus, smoking-cessation counseling should be 
addressed in this population. 

Antibiotic Prescribing for Children with Colds, 
Upper Respiratory Tract Infections, and Bron- 
chitis — Nyquist AC, Gonzales R. Steiner JF, 
Sande MA. JAMA 1998;279( I 1 ):875. 

CONTEXT: The spread of antibiotic-resistant bac- 
teria is associated with antibiotic use. Children 
receive a significant proportion of the antibiotics 
prescribed each year and represent an important 
target group for efforts aimed at reducing unnec- 
essary antibiotic use. OBJECTIVE: To evaluate 
antibiotic-prescribing practices for children 
younger than 1 8 years who had received a diag- 
nosis of cold, upper respiratory tract infection 
( URI ), or bronchitis in tlie United States. DESIGN: 
Representative national survey of practicing physi- 
cians participating in the National Ambulatory 
Medical Care Survey conducted in 1992 with a 
response rate of 73%. SETTING: Office-based 
physician practices. PARTICIPANTS: Physicians 
completing patient record forms for patients 
younger than 18 years. MAIN OUTCOME MEA- 
SURES: Principal diagnoses and antibiotic pre- 
scriptions. RESULTS: A total of 531 pediatric 
office visits were recorded that included a prin- 
cipal diagnosis of cold. URI. or bronchitis. Antibi- 
otics were prescribed to 44% of patients with com- 
mon colds. 46% with URIs. and 75% with 
bronchitis. Extrapolating to the United States. 6.5 



million prescriptions (12% of all prescriptions for 
children) were written for children diagnosed as 
having a URI or nasopharyngitis (common cold), 
and 4.7 million (9% of all prescriptions for chil- 
dren) were written for children diagnosed as hav- 
ing bronchitis. After controlling for confounding 
factors, antibiotics were prescribed more often for 
children aged 5 to 1 1 years than for younger chil- 
dren (odds ratio jOR). 1 .94; 95% confidence inter- 
val |CI]. 1.1 3-3.33) and rates were lower for pedi- 
atricians than for nonpediatricians (OR. 0.57; 95% 
CI. 0.35-0.92). Children aged to 4 years received 
53% of all antibiotic picscnptions, and otitis media 
was the most frequent diagnosis for which antibi- 
otics were prescribed (30% of all prescriptions). 
CONCLUSIONS: Antibiotic prescnbing for chil- 
dren diagnosed as having colds, URIs, and bron- 
chitis, conditions that typically do not benefit from 
antibiotics, represents a substantial proportion of 
total antibiotic prescriptions to children in the 
United States each year. See ihe related arlicle: 
Why Do Physicians Prescribe Antibiotics for 
Children with Upper Respiratory Tract Infec- 
tions? (editorial) — Sclnvariz B. Muinous AG 3nl. 
March SM. JAMA 1998:279(1 1 j:88l-HH2. 

Comparative Efficacy of a Two-Hour Regimen 
of Streptokinase versus Alteplase in Acute Mas- 
sive Pulmonary Embolism: Immediate Clin- 
ical and Hemodynamic Outcome and One- Year 

Follow-Up— Meneveau N. Schiele F. Metz D. 
Valette B. Altali P, Vuillemenot A, et al. J Am 
Coll Cardiol 1998:31(5): 1057. 

OBJECTIVES: This study sought to compare the 
efficacy of 2-h regimens of alteplase and strep- 
tokinase in acute massive pulmonary ciiiholism. 
The primary end point was immediate hemody- 
namic improvement, and secondary end points 
included early clinical efficacy and safety, as well 
as 1 -year clinical outcome. BACKGROUND: Sev- 
eral thrombolytic regimens have been compared 
for the past 10 years in randomized studies, show- 
ing that 2-h infusion regimens of alteplase or uroki- 
nase lead to faster hemodynamic improvement than 
former 12- to 24-h administration protocols in acute 
massive pulmonary embolism. Many trials have 
focused on immediate hemodynamic and angio- 
graphic outcomes, but none has addressed long- 
term follow-up after thrombolysis. METHODS: 
Sixty-six patients with acute massive pulmonary 
embolism (Miller .score > 1 7 and mean pulmonaiy 
artery pressure >20 mm Hg) were randomly 
assigned to receive either a lOO-mg 2-h infusion 
of altepla.se (n = 23) or 1.5 million lU of strep- 
tokinase over 2 h (n = 43). In both groups, hcp- 
ai'in infusion was sl;ined at the end of Ihionibolylic 
infusion and adapted thereafter. Total pulmonary 
resistance was monitored over a 1 2-h iicriod. Pul- 
monary vascular obstruction was assessed 36 to 
48 h after thrombolytic therapy. One-year follow- 
up information included death, cause of death, 
recurrent pulmonary embolism, chronic throm- 
boembolic pulmonary hypertension, stroke, and 



bleeding. RESULTS: Both groups had similar base- 
line angiographic and hemodynamic characteristics 
of severity, with maintained cardiac output in 64 
(97%) of 66 patients. The results (mean ± SD) 
demonsu-ated that despite a faster total pulmonary 
resistance improvement observed at 1 h in the 
alteplase group compared with the streptokinase 
group (33 ± 16% vs 19 16%. p = 0.006). a simi- 
lar hemodynamic efficacy was obtained at 2 h when 
both thrombolytic regimens were completed (38 
± 18% vs 3 1 ± 19%). There was no significant dif- 
ference in either pulmonary vascular obstruction 
at 36 to 48 h or bleeding complication rales. One- 
year event-free survival was similar In both groups, 
as most events were related to concomitant dis- 
eases. CONCLUSIONS: These results suggest that 
a 2-h regimen of streptokinase can be routinely used 
in patients with massive pulmonary embolism and 
maintained cardiac output without obviously com- 
promising efficacy or safety. 

High-Frequency Oscillatory Ventilation in 
Neonatal RDS: Initial Volume Optimization 
and Respiratory IVIechanics — Kalenga M. Bat- 
tisti O. Francois A, Langhendries JP, Gerstmann 
DR, Bertiand JM, J Appl Physiol 1998:84(4): 1 174. 

To determine whether initial lung volume opti- 
mization influences respiratory mechanics, which 
could indicate the achievement of optimal volume, 
we studied 17 premature infants with respiratory 
distress syndrome (RDS) assisted by high-fre- 
quency oscillatory ventilation. The continuous dis- 
tending pressure (CDP) was increased stepwise 
from 6-8 cm H^O up to opfimal CDP (OCDP). 
ie. that allowing good oxygenation with the low- 
est inspired O; fraction. Respiratory system com- 
pliance (Cis) and resistance were concomitantly 
measured. Mean OCDP was 16.5 ± 1.2 cm HiO. 
F|0; could be reduced from an initial level of 0.73 
± 0. 1 7 to 0.33 ± 0.07. However, Cp, (0.45 ± 0. 14 
niL ■ cm H:0 ' ■ kg' at starting CDP point) 
remained unchanged through lung volume opti- 
mization but appeared inversely related to OCDP. 
Similarly, respiratory system resistance was not 
affected. We conclude that there is a marked dis- 
sociation between oxygenation improvement and 
Cr^ profile during the initial phase of lung recruit- 
ment by early high-frequency oscillatory venti- 
lation in infant.s with RDS. Thus optimal lung vol- 
ume cannot be defined by serial Cr^ measurement. 
At the most, low initial C,^ suggests that higher 
CDP will be needed 

Immunizations for International Travelers — 

Thanassi WT. West J Med 1998: 1 (iS( 3): 197. 

Each year more than 45 million Amencans n a\ el 
abroad for work or pleasure, and over 20 niillioii 
of these Havel to njral areas or developing coun- 
tries. While the major medical risks ol inlcrna- 
lional travel are often exaggerated, ihc incidence 
of minor illness is not. Persons going lo Asia, 
Alrica, or l.alin America for 1 month run a 65% 



542 



RESPIRATORY CARF • JULY 1998 VOL 43 NO 7 



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utilization of respiratory care services, assist in determining 
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The Uniform Reporting Manual for Subacute Care 
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and Adjunctive Devices, Mechanical Ventilation, Bronchial 
Hygiene, Diagnostic Tests and Resident Monitoring, 
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Call (972) 243-2272 • Fax (972) 484-2720 



Abstracts 



to 75% chance of becoming ill. although only 1 9; 
will require hospitalization. The 2 most common 
illnesses that affect travelers, which do have immu- 
nizations and are often overlooked by physicians, 
are influenza and hepatitis A. The risk of illness 
to the traveler varies by health and age status, by 
the region to be visited, by the time of year, and 
by the length of the journey. Immunization advice 
for the traveler, therefore, is complicated and is 
best approached in a systematic manner. This arti- 
cle outlines 6 steps to sound immunization advice. 
These steps include ascertaining the traveler's spe- 
cial individual needs, routine immunization sta- 
tus, and routine u~avel immunization status, as well 
as the entry requirements for the country to be vis- 
ited, geographically indicated vaccines, and immu- 
nizations as indicated for extended stays abroad. 

Effects of Inhaled Nitric Oxide in Patients with 
Acute Respiratory Distress Syndrome: Results 
of a Randomized Phase II Trial. Inhaled Nitric 
Oxide in ARDS Study Group— Dellinger RP. 
Zimmennan JL. Taylor RW. Straube RC. Hauser 
DL. Criner GJ, et al. Crit Care Med 1998;26( 1 ): 15. 

OBJECTIVES: To evaluate the safety and phys- 
iologic response of inhaled nitric oxide (NO) in 
patients with acute respiratory distress syndrome 
(ARDS). In addition, the effect of various doses 
of inhaled NO on clinical outcome parameters was 
assessed. DESIGN: Prospective, multicenter. ran- 
domized, double-blind, placebo-controlled smdy. 
SETTING: Intensive care units of 30 academic, 
teaching, and community hospitals in the United 
States. PATIENTS: Patients with ARDS. as 
defined by the American-European Consensus 
Conference, were enrolled into the study if the 
onset of disease was within 72 hrs of random- 
ization. INTERVENTIONS: Patients were ran- 
domized to receive placebo (nitrogen gas) or 
inhaled NO at concentrations of 1.25. 5, 20, 40. 
or 80 ppm. MEASUREMENTS & MAIN 
RESULTS: Acute increases in PaO;. decreases in 
mean pulmonary arterial pressure, intensity of 
mechanical ventilation, and oxygenation index 
were examined. Clinical outcomes examined were 
the dose effects of inhaled NO on mortality, the 
number of days alive and off mechanical venti- 
lation, and the number of days alive after meet- 
ing oxygenation criteria for extubation. A total 
of 177 patients were enrolled over a 14-month 
period. An acute response to treaUnent gas, defined 
as a PaO: increase > 20%. was seen in 60% of the 
patients receiving inhaled NO with no significant 
differences between dose groups. Twenty-four per- 
cent of placebo patients also had ;ui acute response 
to treatment gas during the first 4 hrs. The initial 
increase in oxygenation translated into a reduc- 
tion in the Fio; over the first day and in the intcn 
siiy of mechanical ventilation over the first 4 days 
of treatment, as measured by the oxygenation 
index. Tliere were no differences among the p<X)led 
inhaled NO groups and placebo with respect to 
mortality rate, the number of days alive and off 



mechanical ventilation, or the number of days alive 
after meeting oxygenation criteria for extubation. 
However, patients receiving 5 ppm inhaled NO 
showed an improvement in these parameters. In 
this dose group, the percentage of patients alive 
and off mechanical ventilation at Day 28 ( a post 
hoc analysis) was higher (62% vs44%) than the 
placebo group. There was no apparent difference 
in the number or type of adverse events reported 
among those patients receiving inhaled NO com- 
pared with placebo. Four patients had methe- 
moglobin concentrations >5'7t . The mean inspired 
nitrogen dioxide concentration in inhaled NO 
patients was 1 .5 ppm. CONCLUSIONS: From this 
placebo-controlled study, inhaled NO appears to 
be well tolerated in the population of ARDS 
patients studied. With mechanical ventilation held 
constant, inhaled NO is associated with a sig- 
nificant improvement in oxygenation compared 
with placebo over the first 4 hrs of treatment. An 
improvement in oxygenation index was observed 
over the first 4 days. Larger phase III studies are 
needed to ascertain if these acute physiologic 
impro\ ements can lead to altered clinical outcome. 
See ihc rcUitcil cililnrials: Just Say NO to Inhaled 
Nitric Oxide fur the Acute Respiratory Distress 
Syndrome. Mattliay MA. Pittel JF. Jayr C. Crii 
Care Med 1998:26(1): I: Nitric Oxide Inhala- 
tion in Acute Respiratory Distress Syndrome: It 
Works. But Can We Prore It? Zarol WM. Crit 
Cure Med 1998:26(1)::. 

"Postpolio" Sequelae and Sleep-Related Dis- 
ordered Breathing — Hsu AA. Staats BA. Mayo 
ClinProc 1998;73(3):216. 

OBJECTIVE: To analyze the clinical manifes- 
tations and various types of sleep-related disor- 
dered breathing (SRDB) in patients with a history 
of poliomyelitis and with current "postpolio" 
sequelae (PPS). MATERIAL & METHOD: We 
retrospectively reviewed the medical records of 
108 consecmive patients with PPS and sleep dis- 
turbances encountered during an 1 1-yr period at 
Mayo Clinic Rochester and abstracted the fea- 
tures of acute polio. PPS. and results of sleep eval- 
uation (overnight oximetry or polysomnography). 
Only those patients who were not receiving ven- 
tilatory support were included in the study. 
RESULTS: The features of PPS were dyspnea, 
fatigue, new weakness, and musculoskeletal pain. 
Of the 108 patients. 35 fulfilled the inclusion cri- 
teria. Sleep evaluations revealed 3 general types 
of disturbances: obstructive sleep apnea (Group 
O. n = 19); hypovennlation (Group H. n = 7); and 
both (Group OH, n = 9). The mean apne;i/hypop- 
nea index was 37. 4. and 16/hr in patients in 
Groups O. H. and OH, respectively (p < 0.05 ), and 
the mean arterial carbon dioxide tension was 39, 
60. and 55 mm Hg in these respective study groups 
(p < ().()5). The overall mean age at onset of symp- 
toms of SRDB was 47 years, and the mean latent 
period after acute polio was 37 years. Hyper- 
somnolence was the commonest SRDB symptom. 



present in 32 of the 35 patients. Snoring was noted 
in 100% of patients in Group 0. 0% in Group H. 
and 67% in Group OH. Patients in Group O were 
obese and had normal lung function. Patients in 
Group H tended to have normal weights and a fiis- 
tory of diffuse neurologic deficits involving the 
trunk during the acute episode of polio. Scolio- 
sis, restricted lung function, cor pulmonale, and 
decreased maximal respiratory pressures were 
common in patients in Group H. Patients in Group 
OH had overlapping features of those in Groups 
O and H. CONCLUSION: In patients with PPS. 
we identified 3 patterns of sleep disturbances — 
obstructive sleep apnea, hypoventilation, and a 
combination of both. These groups are charac- 
terized by clinical features and by results of arte- 
rial blood gas determinations, overnight oxime- 
try, and polysomnography. SRDB is a late sequela 
of poliomyelitis, and clinical evaluation should 
include information about sleep. 

Declining Morbidity and Mortality among 
Patients with Advanced Human Immunode- 
ficiency Vims Infection. HIV Outpatient Study 
Investigators — Palella FJ Jr, Delaney KM. Moor- 
man AC. Loveless MO. Fuhrer J. Satten GA. et 
al. N Engl J Med 1998;338( 13):853. 

BACKGROUND & METHODS: National 
surveillance data show recent, marked reductions 
in morbidity and mortality associated with the 
acquired immunodeficiency syndrome (AIDS). 
To evaluate these declines, we analyzed data on 
1255 patients, each of whom had at least one 
CD4-I- count below 1(X) cells/mm' who were seen 
at 9 clinics specializing in the u-eatment of human 
immunodeficiency virus (HIV) infection in 8 U.S. 
cities from January 1994 through June 1997. 
RESULTS: Mortality among the patients declined 
from 29.4/100 person-yrs in the first quarter of 
1995 to 8.8/100 in the second quarter of 1997. 
There were reductions in mortality regardless of 
sex. race. age. and risk factors for transmission 
of HIV. The incidence of any of 3 major oppor- 
tunistic infections (Pneumocystis carinii pneu- 
monia. Mycohucteriiim avium complex disease, 
and cytomegalovirus retinitis ) declined from 21.9 
/lOO person-yrs in 1994 to 3.7/100 person-yrs by 
mid- 1997. In a failure-rate model. increa.ses in the 
intensity of antiretroviral therapy (classified as 
none, monotherapy, combination therapy with- 
out a protease inhibitor, and combination therapy 
with a protease inhibitor) were associated with 
stepwise reductions in morbidity and mortality. 
Combination antiretroviral therapy was associ- 
ated with the most benefit; the inclusion of pro- 
tease inhibitors in such regimens conferred addi- 
tional benefit. Patients with private insunuice wens 
more often prescribed protease inhibitors and had 
lower mortality rates than those insured by Medi- 
care or Medicaid. CONCLUSIONS: The recent 
declines in morbidity and mortality due to AIDS 
are attributable to the use of more intensive 
antiretroviral therapies. 



544 



Ri-spiRATORY Care • July 1998 Vol 4.^ No 7 



Haniiillii' 



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Editorial 



Professionalism, Respiratory Care Practice, and Physician Acceptance 
of a Respiratory Consult Service 

Dean R Hess PhD RRT 



The traditional role of the respiratory therapist was task 
oriented; in this role the therapist skillfully implemented the 
procedures prescribed by the physician. TTiis model functioned 
well for many years and was seldom questioned — p;irticularly 
in a fee-for-service environment in which respiratory care pro- 
cedures were lucrative for hospitals. It has been known for 

See the Original Study on page 549 

many years that a pattern of over-ordering of respiratory ther- 
apy occurs in many hospitals and that significant reductions 
in the volume of respiratory therapy procedures could be 
achieved with no adverse effect on patient outcomes. ' Sim- 
ilarly, a pattern of misallocation of respiratory care was 
described in which patients received either therapy that was 
not indicated or indicated therapy was not prescribed.- Con- 
current with the increasing recognition of the common mis- 
allocation of respiratory care, there has been increasing pres- 
sure to control health care costs. There has also been increased 
training of respiratory therapists in patient assessment and a 
desire of therapists to evolve beyond a task-oriented role to 
an increased professional role at the bedside. 

The Traditional Model Results in Misallocation 

The traditional model (ie, the respiratory therapist perfonns 
procedures as specifically prescribed by a physician) results 
in misallocation for several reasons.' First, there may be insuf- 
ficient understanding of respiratory care by those who pre- 
scribe the therapy. Although any physician can prescribe res- 
piratory care, many never receive any specific instruction in 
ordering it. Second, the respiratory care needs of patients are 
variable and the prescribing physician may not be available 
to change the prescription when the patient's condition changes. 
The respiratory care prescription may be overlooked as the 
physician pays attention to other important needs of the patient. 
I am certain that respiratory care veterans remember many 
orders that were written at the time of patient admission and 
remained unchanged for days while the patient's condition 



improved and the diminishing need for intensive respiratory 
care (or perhaps any respiratory care) was overlooked by the 
prescribing physician. 

Respiratory Therapists Can Improve Allocation 

In the past 10 years, there has been increasing use of res- 
piratory therapists as consultants. This has been achieved by 
use of therapist-driven protocols, also known as patient-driven 
protocols, evaluate-and-treat programs, and respiratory ther- 
apy consult services.' With these approaches, the physician 
orders the protocol rather than the specific therapy. Within 
the boundaries set by these medical-staff-approved protocols, 
a respiratory therapist assesses the patient, develops a respiratory 
care plan, implements the therapy, assesses the patient's 
response, and modifies the caie plan as appropriate. Tliere have 
been several reports of the effectiveness of such programs,"*' 
and arguably the most sophisticated may be that at the Cleve- 
land Clinic."" 

There are at least two issues of concern to physicians 
related to respiratory care protocols. First is a concern related 
to physician autonomy, in which the prescribing physician 
desires absolute control over all aspects of the patient's care. 
In many cases, this relates to a lack of confidence by the physi- 
cian in the skills of the respiratory therapist. A second issue 
relates to the potential impact of respiratory care protocols 
on the training of house officers in academic centers. There 
is a concern among some physician educators that a skill- 
fully implemented respiratory care protocol will decrease the 
opportunity for house officers to learn how to order respi- 
ratoiy care. I find this iirgument a p;iradox. given that the avail- 
able evidence of the misallocation of respiratory care sug- 
gests that physicians may not learn how to order respiratory 
care very well. In this issue of the Journal, Stoller and Mich- 
nicki '" report the results of a survey of house officers' atti- 
tudes regarding the impact of their respiratory therapy con- 
sult service. They report that almost all house staff surveyed 
(97%) regaided the respiratoi7 therapy consult sci-vice as help- 
ful to the care of their patients. The majority, although only 
,'i6'7f , felt that the consult service enhanced the house staff's 



.';46 



RH.SPIRATORY CARH •JUl.Y 1998 VOL 4.^ NO 7 



Professionalism. Rhspiratory Care Practice, and Physician Acceptance 



knowledge of respiratory care ordering. 

Partnership, Professionalism, & Protocols 

What can be done to improve physician acceptance of res- 
piratory c;ire protocols? I believe that this can occur only when 
respiratory therapists develop partnerships with physicians 
and when respiratory therapists conduct themselves as pro- 
fessionals at the bedside. An environment must be developed 
that values the therapist as a consultant. This begins with com- 
munication. The therapist-as-consultant role does not happen 
simply because a respiratory therapy protocol is implemented. 
In fact, the successful implementation of protocols may depend 
upon a prior respect of physicians for respiratory therapists 
based upon professional interactions at the bedside. One might 
argue that respiratory therapy protocols are unnecessary in 
an environment where there is free and open commimication 
between physicians and respiratoi7 therapists. In fact, the ben- 
efit of forced interactions between respiratory therapists and 
physicians has been demonstrated." '- At the Massachusetts 
General Hospital, we have no structured respiratory care pro- 
tocols. However, our respiratory therapists communicate freely 
and frequently with physicians, the opinions of the respira- 
tory therapists are often consulted and respected, and the res- 
piratory care plans of patients often reflect the suggestions 
of the respiratory therapists. 

A mistake that I have noted with the implementation of 
respiratory therapy protocols is a tendency for therapists to 
view the protocol as a task rather than a consultation. This 
can damn the success of the protocol. Strict adherence to pro- 
tocol instructions with little thought regarding the decisions 
that are made is task oriented and unprofessional. This will 
not engender the confidence of physicians in either the pro- 
tocol or the therapist. I cannot stress enough the importance 
of the therapist acting as a consultant — whether or not pro- 
tocols are used. Respiratory therapists can be consultants with- 
out protocols and protocols do not assure a consultative role. 
Carefully reasoned suggestions by a respiratory therapist with 
the needs of the patient in mind will elevate the respect of the 
physician for the therapist — even if the physician does not 
agree with the therapist's suggestions (physicians do not always 
agree with their physician consultants, either). Protocols can 
provide a framework to assist with the proper allocation of 
respiratory care, but the protocol should not be a substitute 
for thinking and communication. 

I do not believe that respiratory care protocols and physi- 
cian education are incompatible. An important role of res- 
piratory therapists is to teach others — including physicians. 
Respiratory therapists are the experts on respiratory care and 
should be intimately involved in teaching physicians. This 
can occur through fonnal classroom teaching or. more impor- 
tantly, at the bedside. A protocol should not be implemented 
in a vacuum. The therapist's assessment and care plan should 



be openly communicated to the prescribing physician. The 
physician should understand the rationale for the care plan 
that is chosen and agree with that plan. In this way the deci- 
sions of the respiratory therapist become a model for the physi- 
cian-in-training. An environment should exist in which the 
physician is a partner with the respiratory therapist in select- 
ing the best care for the patient. 

Therapist Responsibility 

The responsibility for successful implementation of res- 
piratory care protocols rests primarily with the therapist at the 
bedside. The medical director who champions the role of res- 
piratory therapists and who promotes the protocol among the 
medical staff is important. A progressive and receptive med- 
ical staff is important. The support of nurses and other health 
professionals is important. However, the professional respiratory 
therapist at the bedside assessing the patient, making the cor- 
rect decisions, and communicating with other members of the 
health care team adds value — that's what makes the proto- 
col successful. 



Dean R Hess PhD RRT 

Assistant Professor of Anesthesia 

Harvard Medical School 

Assistant Director of Respiratory Care 

Massachusetts General Hospital 

Boston, Massachusett 



REFERENCES 



1 Zibrak JD. Rossetti P. Wood E. Effect of reductions in respiratory 
therapy on patient outcome. N Engl J Med l986;-1LS(.'i):292-29.'). 

2. Kester L. Stoller JK. Ordering respiratory care services for hospi- 
talized patients: practices of overuse and underuse. Cleve Clin J Med 
1992;.'i9(6);.'i81..'i85. 

-^. Stoller JK, The rationale for therapist-driven protocols (review). Respir 
CareClinN Am 1996;2(1 ):l-14. 

4. Nielsen-Tietsort J. Poole B, Creagh CE, Repsher LE. Respiratory 
care protocol: an approach to in-hospital respiratory therapy. Respir 
Care 1981;26(.'i):4,W-4.^6. 

."i. Torringlon KG. Henderson CI. Perioperative respiratory therapy 
(PORT): a program of perioperative risk assessment and individu- 
alized postoperative care. Chest 19S8:9.^(5):946-951. 

6. Shapiro BA. Cane RD, Peterson J. Weher D. Authoritative medical 
direction can assure cost-beneficial bronchial hygiene therapy. Chest 
1988;9.^(.S): 1038- 1042. 

7. Shrake KL. Scaggs JE. England KR. Henkle JQ. Eagleton LE. 
Benefits associated with a respiratory care assessment-treatment 
program: resultsof a pilot study. Respir Care 1994;39(7):7 15-724. 

8. Stoller JK. Haney D, Burkhart J. Fergus L. Giles D, Hoisington E. 
et al. Physician-ordered respiratory care vs physician-ordered use of 
a respiratory therapy consult service: early experience at the Cleve- 
land Clinic Foundation. Respir Care I993;38( 1 1 ): 1 143-1 LS4 



RESPIRATORY CARE • JULY 1998 VOL 4.^ NO 7 



547 



Professionalism, Respiratory Care practice, and Physician Acceptance 



Stoller JK, Skibinski CI. Giles DK. Kester EL. Haney D. Physician- 
ordered respiratory care versus physician-ordered use of a respira- 
tory therapy consult service: results of a prospective observational 
study. Chest 1 996; 1 1 0( 2 ):422-429. 

Sloller JK. Michnicki I. Medical house staff impressions regarding 
ilie impact of a respiratory therapy consult service. Respir Care 
I99S;4.^(7):549-551. 

Hart SK, Dubbs W. Gil A, Myers-Judy M. The effects of therapist- 
evaluation of orders and interaction with physicians on the appro- 
priateness of respiratory care. Respir Care I989;34(3):185-190. 



1 2. Ely EW. Baker AM. Dunagan DP. Burke HL. Smith AC. Kelly PT. 
et al. Effect of the duration of mechanical ventilation of identifying 
patients capable of breathing spontaneously. N Engl J Med 
1996;.33.'i( 25); 1864- 1869. 



Correspondence: Dean R Hess PhD RRT. Respiratory Care Services. 
Ellison 401, Massachusetts General Hospital, ."iS Fruit Street, Boston MA 
021 14; e-mail; dhess@partners.org. 



548 



RESPIRATORY CARE • JULY 1998 VOL 4.'^ NO 7 



Original Contributions 



Medical House Staff Impressions Regarding the Impact of a 
Respiratory Therapy Consult Service 

James K Stoller MD and Irene Michnicki RRT 

BACKGROUND: Although the Respiratory Therapy Consult Service (RTCS) has been shown 
to be effective in enhancing the allocation of respiratory care services, the criticism has been lodged 
that allocating algorithm-based decision-making to respiratory care practitioners detracts from 
physicians' in-training knowledge of respiratory care. To assess whether medical house staff regarded 
a well-established RTCS to be clinically and educationally helpful, we undertook a survey of house 
staff attitudes regarding the impact of this service on both patient care and house staff skill in order- 
ing respiratory care. METHODS: A single-page, 6-question instrument was distributed at a reg- 
ularly scheduled meeting of the Cleveland Clinic Foundation medical house staff. The questions 
posed were: ( 1 ) Do you know what the RTCS is? (2) Do you feel the RTCS is helpful or detrimental 
to the care of your patients? (3) Do you feel it has enhanced or detracted from your knowledge of 
respiratory care ordering? (4) Do you have a Respiratory Therapy Consult handbook? (5) Have 
you read it? (6) Have you found it helpful? RESULTS: Of a total of 95 available members of the 
medical house staff, 62 attended the meeting (65% ), and 41 submitted responses (66% of atten- 
dees). Of the 41 respondents, 95% were aware of the RTCS. Similarly, 97% regarded the RTCS 
as being helpful to the care of their patients. Of 34 respondents, 56% felt that the RTCS enhanced 
the house stafTs knowledge of respiratory care ordering, 32% felt that the Consult Service detracted 
from the house staffs knowledge, and 12% indicated that the RTCS had neither effect. Twenty- 
seven percent (11/41) indicated that they had an RTCS handbook, 19% (7/36) had read the hand- 
book, and 33% (5/15) found it helpful. CONCLUSIONS: We conclude that the majority of respond- 
ing house staff at the Cleveland Clinic Foundation were aware of the RTCS, suggesting successful 
institutional notification about the service. Similarly, almost all house staff regarded the Consult 
Service as being helpful in caring for their patients (97% ), while 56% felt that the Respiratory Ther- 
apy Consult Service enhanced the house staffs knowledge of respiratory care ordering. Further 
study is required to examine whether these impressions about the impact of the RTCS are sup- 
ported by direct measure of the house staffs knowledge of respiratory care ordering. [Respir Care 
1998;43(7):549-55 1 ] Key words: Respiratoiy therapy consult senices, house staff, protocols. 

Introduction ^^^^ costs.' ' However, the use of respiratory care protocols 

(in whicli respiratory care practitioners prescribe care based 
Respiratory care protocols have gained wide acceptance ^^ approved guidelines and/or algorithms) has engendered 
based on emerging evidence that they improve the allocation ^ome concern by medical educators that respiratory care pro- 
of respiratory care services, enhance medical outcomes, and tocols and use of a respiratory therapy consult service will 

detract from house officers" education regarding the appro- 
priate use of respiratory care therapies for their patients. 



James K Stoller MD and Irene Michnicki RRT: Department of Pulmonary 
and Critical Care Medicine. Section of Respiratory Therapy, Cleveland Clinic 
Foundation, Cleveland, Ohio 

A version of this paper was presented by Ms Michnicki at the Respiratory 
Care Open Forum during the American Association for Respiratory Care's 



See THE RELATED EOITORLAL ON PAGE 546 



IntetTtational Respiratory Congress, December 6-9, 1997 in New Orieans. ^s part of an ongoing assessment of the efficacy and impact 

Louisiana. of respiratory care protocols in our institution, the current study 



was undertaken to determine medical house officers" impres- 
sions of a long-standing Respiratory Therapy Consult Service 
Euclid Ave, Cleveland OH 44195; e-mail: stollej@cesmtp.ccforg. (RTCS). To assess whether or not medical house staff regarded 



Reprints & Correspondence: James K Stoller MD. Department of Pulmonary . ,- , ,• r. • t^i ^ i (^ ■ 

1 /- .■ 1 /- L J- ■ nv I A nn ^1 i j ^r r: ■ n^AA sions ot 3 loug-standing Respiratory Therapy Consult Service 
and Cntical Care Medicine. Desk A-90, Cleveland Clinic Foundation, 9500 "^ e t- j t-j 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 549 



Medical House Staff Impressions 



a well-established respiratory therapy consult service to be clin- 
ically and educationally helpful, we undeilcxik a survey of house 
staff attitudes regarding the impact of this service on both patient 
care and house staff skill in ordering respiratory care. 

Methods 

We used a single page, 6-question survey instrument that 
was administered at a regularly scheduled didactic meeting 
of the Cleveland Clinic medical house staff. Plans to admin- 
ister the survey were not announced before the meeting, at 
which the study investigators distributed the questionnaires 
with introductory remarks emphasizing our desire for can- 
did feedback on the RTCS. The questions posed were: ( 1 ) 
Do you know what the RTCS is? (2) Do you feel that the 
RTCS is helpful or detrimental to the care of your patients? 
(3) Do you feel the RTCS has enhanced or detracted from 
your knowledge of respiratory care ordering? (4) Do you have 
an RTCS handbook? (5) Have you read the handbook? (6) 
Have you found the handbook helpful? 

As part of routine house staff orientation in July of each 
year, each house officer had received a copy of the hand- 
book that describes the RTCS and contains the algorithms 
that guide respiratory care ordering in our hospital. As pre- 
viously described."*^ the algorithms are branched logic dia- 
grams that are indexed to specific respiratory signs and symp- 
toms and are based on American Association for Respiratory 
Care Clinical Practice Guidelines.^ Because the RTCS has 
been mandated for use on most adult, non-ICU inpatients 
in the Cleveland Clinical Hospital, house officers frequently 
interact with respiratory care practitioners as they apply the 
RTCS algorithms. 

Results 

Of a total of 95 available members of the medical house 
staff. 62 attended this regularly scheduled meeting (65%) and 
41 submitted responses (66% of attendees, 43% of all med- 
ical house officers). Of the 41 respondents, 95% were aware 
of the RTCS (Fig. I ). Similarly, 97% regarded the RTCS as 
being helpful to the care of their patients. Of the 34 respon- 
dents to Question 3 (Do you feel that the RTCS has enhanced 
or detracted from your knowledge of respiratory care order- 
ing?). 56% felt that the RTCS enhanced the house start's knowl- 
edge of respiratory care ordering. 32'/r felt that the RTCS 
detracted from the house staffs knowledge, and 12% indi- 
cated that the RTCS had neither effect. Twenty-seven per- 
cent (1 1/41 ) indicated that they had the handbook. 19% (7/36) 
had read the handbook, and 33'/, (5/15) found it helpful. 

Discussion 

Although contrary and perhaps suiprising to critics' expec- 
tations, our results show that most participating medical house 




Fig. 1. [Histogram distribution of medical house officers' responses 
to the 6-question instrument: Question 1 . Do you know what the 
Respiratory Therapy Consult Service (RTCS) is? Question 2. Do 
you feel the RTCS is helpful (yes) or detrimental (no) to the care of 
your patients? Question 3. Do you feel the RTCS has enhanced 
(yes) or detracted from (no) your knowledge of respiratory care? 
Question 4. Do you have an RTCS handbook'' Question 5. Have 
you read the RTCS handbook? Question 6. Have you found the 
RTCS handbook helpful? ■= yes responses: □= no responses: 
□ = neither or neutral responses. The total number of respondents 
to each question is indicated above each bar. 



officers regarded the RTCS as enhancing the respiratory care 
their patients received and enhancing their own knowledge 
of respiratory care ordering. At the same time, almost one 
third of respondents felt that the RTCS detracted from their 
knowledge of respiratory care — an issue that raises concerns 
about the possible undesirable effects of a respiratory ther- 
apy protocol program. 

Although data about the impact of protocols on medical 
trainees" education are sparse, our results are consistent with 
findings from a preliminary report by Messenger.^ Specifi- 
cally, in a survey of 1 94 physicians to which 26 of .54 respon- 
dents (48%) were house officers. Messenger reported that many 
responding physicians regarded a respiratory care protocol 
program as increasing the timeliness (48%), quality (50%). 
and appropriateness (56%^) of respiratoiy care delivered in the 
hospital. To our knowledge, no other study has examined the 
impact of respiratory care protocols on house officers' knowl- 
edge of respiratory care. 

In the context that this is the first study to examine this issue, 
several shortcomings of this research are noteworthy. First. 
as with all survey-based research in which response rates are 
incomplete, we cannot exclude the possibility that respondents 
comprised a biased sample and. therefore, that the perceptions 
we recorded were not representative of all medical house offi- 
cers. Specifically, our findings are based on responses from 
66% of the attendees at the meeting, who comprised 43% of 
all medical house officers at the Cleveland Clinic. At the same 
time, because the survey was not announced Ixibirhand, except 
tor the Linlikcly possibility that conscientious attendance at 



550 



RESPIRATORY CARF •JUI.Y 1998 VOI. 43 NO 7 



Medical House Staff Impressions 



house staff meetings is somehow tied to favoring the RTCS, 
we do not suspect that this respondent sample was system- 
atically biased in favor of respiratory care protocols. Also, 
despite our explicit request for candid responses, even if unflat- 
tering, we also cannot discount the possibility that respondents 
were inclined to provide favorable impressions. 

Another important limitation of this initial study is that we 
elicited only house officers" impressions about the impact of 
the RTCS but did not actually assess house officers" exper- 
tise in ordering respiratory care services. As such, it is pos- 
sible that the generally favorable impression about the impact 
of the RTCS on house staff knowledge of respiratory care is 
discordant with actual knowledge-based peifonnance in order- 
ing appropriate respiratory care, hideed, addressing this issue 
requires comparing the actual knowledge base of respiratory 
care ordering by two groups of house officers: a group that 
has experienced a respiratory care protocol service versus a 
group that has not. Because the RTCS has been available in 
our institution since 1992 and medical house officers have 
been exposed continuously to this service since that time, an 
intramural comparison is not possible. Rather, we have ini- 
tiated a multi-institutional study to compare performance in 
ordering respiratory care by two matched groups of house offi- 
cers, one at our institution and the comparative group at an 
academic institution in which a respiratory care protocol pro- 
gram has not been initiated to date. 

Finally, it will be important to more fully understand the 
specific reasons that 32% of the respondents felt that the RTCS 
detracted from their educational experience and whether this 
impression is supported by shortcomings of actual respira- 
tory care knowledge. 

Conclusions 

In summary, our results show that most responding med- 
ical house officers in our institution regarded the RTCS favor- 
ably, with 97% regarding the RTCS as enhancing the clin- 
ical care provided to their patients and 56% reporting that the 
RTCS enhanced their knowledge of respiratory care order- 
ing. To our knowledge, this is the first study to address this 
important educational question. Although our overall results 
challenge the view that a respiratory care protocol service 
detracts from house officers" education, this study clearly rep- 



resents only an initial analysis of this issue, and additional study 
is needed in order to confinn and extend these findings. Specif- 
ically, before house staff acceptance of respiratory care pro- 
tocols can be considered firm, reproducibly favorable results 
from studies of other house staff groups are needed. Even more 
broadly, demonstrating physician acceptance of respiratory 
caie protocols will require sampling a fuller spectnim of physi- 
cians with whom respiratoi^ c;ire practitioners interact, namely 
attending physicians, fellow physicians, and both private and 
academic physicians. 

It is important to note that our finding that support for the 
educational benefits of the RTCS was not unanimous raises 
concern and underscores the need to better understand poten- 
tial detrimental effects of a respiratory care protocol service. 

To address the shortcomings of the current research, a larger 
study with a more complete response rate is needed, ideally 
surveying house officers in multiple disciplines and in mul- 
tiple institutions. Furthermore, to extend the analysis beyond 
opinion alone, the actual impact of a respiratory care proto- 
col service on house officers" education should be assessed 
in studies that test house officers" knowledge of respiratory 
care ordering. 

REFERENCES 



1. Stoller JK. The rationale fnrtlnerapist-driven protocols. RespirCare 
Clin N Am 1996:2(1 ): 1-14. 

2. Stoller JK, Skitiinski CI, Giles D. Kester EL. Haney D. Physician- 
ordered respiratory care vs phy.sician-ordered use of a respiratory ther- 
apy consult service: results of a prospective observational study. Chest 
1996:1 10( 2 ):422-429. 

.^ Kollef MH. Shapiro SD, Silver P. St John RE, Prentice D, Sauer S, 
et al. A randomi/ed, controlled trial of protocol-directed versus physi- 
cian-directed weaning from mechanical ventilation. Crit Care Med 
1997:25(4):567-.'574. 

4. Kester L. Stoller JK. A primer on therapist-driven protocols. Clin 
PulmMed 1994:1:93-99. 

-S. Stoller JK, Haney D. Burkhart J. Fergus L. Giles D, Hoisington E, 
et al. Physician-ordered respiratory care vs physician-ordered use of 
a respiratory therapy consult .service: early experience at The Cleve- 
land Clinic. RespirCare 1993:38(11): 1143-1 154. 

6. American Association for Respiratory Care. The AARC Clinical Prac- 
tice Guidelines. RespirCare I991;36(I2):1398-1426. 

7, Messenger R. Physicians' perceptions of a protocol program (abstract). 
RespirCare 1997:42(1 1): 1108. 



RESPIRATORY CaRE • JULY 1998 "VOL 43 NO 7 



551 



Two-Tiei ed Response for Emergency Airway Management by 
Respiratory Therapists and Anesthesiologists 

John D Hussey MBA RRT, Michael J Bishop MD, Lewis Massey, S Lakshminarayan MD, 
James Joy MD, and Jennifer Finley MD 



INTRODUCTION: Out-of-operating-room intubations carry the potential for serious morbidity 
and mortality and require the around-the-clock presence of personnel trained in emergency air- 
way management. METHODS: We established a hybrid model for response to airway prob- 
lems of an acutely ill patient population; in this model, respiratory therapists handled emer- 
gent intubations with telephone back up from anesthesiologists whereas the anesthesiologist came 
in to the hospital to handle urgent intubations. Emergent intubations are cases in which the patient 
was expected to require intubation in < 30 min. The model is based on an assessment that demon- 
strated that the most complex intubations are urgent rather than emergent. Following the train- 
ing described, the model was put in place, and the results of the first 18 months are reported. 
RESULTS: One hundred sixty four out-of-operating-room intubations were required, includ- 
ing 89 cardiac arrest patients and 75 noncardiac arrest patients. Respiratory therapists intu- 
bated the majority of cardiac arrest patients whereas the majority of nonarrest situations were 
intubated by anesthesiologists. Intubation was successful in 162 of 164 patients; 2 failures occurred 
in cardiac arrest situations with a physician present but no anesthesiologist immediately avail- 
able. However in both cases, the anesthesiologist who arrived also could not intubate. CON- 
CLUSIONS: This model permits the anesthesiologist to be available for the majority of intu- 
bations in the noncardiac arrest situation in which medical management and pharmacologic 
therapy are often required; whereas respiratory therapists perform the majority of intubations 
during cardiac arrest. This model is successful and resulted in economic savings. [Respir Care 
1998;43(7):552-556] Key words: Intubation, algorithms, role of respiratory therapist. 



John D Hussey MBA RRT and Lewis Massey. Department of Respiratory 
Therapy, VA Puget Sound Health Care System — Seattle Division; 
Michael J Bishop MD, Department of Anesthesiology, VA Puget Sound 
Health Care System — Seattle Division, and the Department of Anesthesi- 
ology and Division of Pulmonary and Critical Care Medicine, University 
of Washington; S Lakshminarayan MD. Department of Medicine, VA 
Puget Sound Health Care System — Seattle Division, and Division of Pul- 
inonary and Critical Care Medicine, University of Washington; James Joy 
MD and Jennifer Finley MD. Department of Anesthesiology, VA Puget 
Sound Health Care System — Seattle Division, and Department of Anes- 
thesiology, University of Washington; Seattle, Washington. 



Supported in part by the Offic 
meni of Veterans Affairs. 



of Research and Development. Depart- 



A version of this paper was presented by Mr Hussey during the annual 
Open Forum at the 4.Vd International Respiratory Congress. December 3- 
6. 1997. in New Orleans. Louisiana. 

Correspondence & Reprints: John D Hussey MBA RRT, Deparlmcnl of 
Respiratory Therapy. VA Puget Sound Health Care System — Seattle 
Division, 1 660 S Columbian Way ( 1 1 1 B ). Seattle WA 98 1 08. 



Introduction 

Because of the potential for airway emergencies to result 
in serious morbidity and mortality, an acute care hospital 
requires personnel trained in emergency airway management 
to be available at all times. In the acute care facilities with 
anesthesiology training programs, a physician trained in anes- 
thesiology or emergency medicine is present at the hospital 
and responsible for emergency airway management in more 
than 90% of institutions surveyed.' Although respiratory ther- 
apists all receive some training in endotracheal intubation. - 
the extent of ongoing practice is variable and therapists do 
not routinely perform inttibations in many hospitals — only 
]% of hospitals with anesthesiology training programs used 
therapists for floor intubations.' A major impediment to the 
more widespread practice of intubation by respiratory ther- 
apists is that many patients requiring tracheal intubation have 
complex medical problems that may icquiie pharmacologic 
therapy during the intubation. 



5,52 



RH.SPIRATORY CARH • JULY 1998 VOL 4.^ NO 7 



TWO-TlERED RESPONSE FOR EMERGENCY AIRWAY MANAGEMENT 



Although hospitals with anesthesiology training programs 
mostly use physicians for emergency airway management, 
the vast majority of hospitals do not have training programs. 
Tlie number of anesthesiology training programs in the United 
States has declined in each of the last three years and will 
decline again this July ( 1998) to approximately 140. only a 
small minority of hospitals in the country.' Many of the exist- 
ing programs have cut back on the number of residents being 
trained, limiting staffing. Reductions in available anesthesia 
staffing at our 280-bed medical center led us to evaluate pos- 
sible models to ensure safe and timely care of airway emer- 
gencies without requiring aiound-the-clock presence of a physi- 
cian trained in airway management. Our review of possible 
models in the literature suggested that properly trained non- 
physicians could intubate the trachea with a success rate 
equal to or better than most physicians.'"' These data came 
from experience both with paramedics in the out-of-hospi- 
tal setting and respiratory care practitioners in the hospital."* 
^ However, much of the literature refers to intubations for car- 
diac arrests, where no pharmacologic intervention to 
produce muscle relaxation or sedation is necessary. In 
reviewing our out-of-operating-room intubations, we found 
that many were in unstable but not aiTested patients with high 
risk of deterioration during intubation. These patients 
included postcardiac surgery patients, bone marrow transplant 
patients, postaortic surgery patients, post-thoracotomy patients, 
and patients with chronic obstructive pulmonary disease 
(COPD) or cardiac failure. 

We hypothesized that a hybrid two-level model of emer- 
gency airway care would result in safe management of air- 
ways with acceptable outcomes. This hybrid model was 
designed to have the respiratory therapist intubate the trachea 
during cardiac arrest situations with an anesthesiologist 
available via telephone for consultation. Patients requiring 
intubation for respiratory failure, airway maintenance, or other 
progressive conditions were deemed to be more complex sit- 
uations and an anesthesiologist was routinely present for such 
cases. 

We describe the structure of the program and report the 
results of the first 1 8 months of the program. 

Methods 

Airway management and tracheal intubation training were 
initiated through a program within the operating room (O.R.) 
under the supervision of the Department of Anesthesiology. 
All therapists on staff rotated through the O.R. and were 
required to demonstrate a series of cognitive and procedu- 
ral milestones (Table 1 ). Prior to patient contact, each ther- 
apist reviewed basic head positioning, blade placement, and 
tube positioning using a mannequin. Every O.R. intubation 
was evaluated by the attending anesthesiologist using stan- 
dardized criteria. Criteria included head positioning, place- 
ment of the tube, and assessment of tube placement. Strengths 



Table I . Required Skills for Certification 



Cognitive 



Procedural 



Access airway for difficult intubation 
Describe views of larynx 



Understand indications and 
contraindictions for muscle relaxants 



Plan for failed intubation 



Identification of successful intubation 

1. Using bulb syringe 

2. Using end-tidal COi 



Bag-and-mask ventilation 

Application of cricoid pressure 



Intubation using Macintosh 
and Miller blades 



Intubation over a gum elastic 
bougie 



Placement of laryngeal mask 
airway 



and weaknesses were reviewed immediately to support 
improvement and a written assessment produced. In-service 
sessions, lectures, and written resource materials were used 
to support the training. A second level of educational support 
was accomplished through anesthesia-supervised elective and 
emergent intubations outside the O.R. Final certification 
included passing a written test. 

Although we had initially established 10 as the minimum 
number of intubations required in the O.R. based in part on 
a literature report using 12 as a miniinum,'' the minimum num- 
ber actually perfomied by any therapist prior to certification 
ranged from 15 to 46, with a mean (SD) 31(17). The variability 
in the number of intubations required resulted from differ- 
ing levels of prior training and experience as well as varying 
rates of acquisition of the required knowledge and skills. 

Our model consisted of defining airway care as either urgent 

Need for Tracheal Intubation Identified 




Emergent 
n response needed) 



Anesthesiologist 
notified 



Urgent 
n delay acceptable) 



Anesthesiologist notified 
and proceeds to hospital 





Anesthesiologist 

performs airway 

management or 

supervises Respiratory 

Therapist 



Respiratory Therapists 

manages airway and intubates. 

Anesthesiologist provides 

consultation by phone 



. Patient 
deteriorates 



Patient remains 

stable until 
anesthesiologist 



Fig. 1 . The algorithm for tracheal intubations out of the operating room. 



Respiratory Care • July 1998 Vol 43 No 7 



553 



Two-TiERED Response for Emergency Airway Management 



or emergent based on whether the patient was expected to 
require endotracheal intubation within 30 min. The decision 
tree for intubation is depicted in Figure 1. For emergent intu- 
bations, the respiratory therapist could proceed immediately 
whether an anesthesiologist was immediately available. Simul- 
taneously, the anesthesiologist was paged and alerted to the 
situation. The anesthesiologist was thus available for phone 
consultation in case of intubation difficulty and could pro- 
ceed to the hospital if further assistance was needed. The anes- 
thesiologist could also consult with the medical house offi- 
cer at the bedside via cell phone. 

For urgent intubations, the anesthesiologist was called to 
the hospital and the therapist remained with the patient until 
the anesthesiologist arrived. Intubation was then performed 
either by the therapist under the direction of the anesthesi- 
ologist or by the anesthesiologist. The decision was based on 
the assessment by the anesthesiologist. The anesthesiologist 
directed all pharmacologic interventions. 

Training also included providing the therapists with options 
in case of initial failure to intubate. The therapists were trained 
to use both Macintosh and Miller laryngscopic blades, 
instructed to use a smaller diameter tube if visualization was 
a problem, or to place a gum bougie and to feed a tube over 
the bougie. Finally, therapists were shown how to place a laryn- 
geal mask airway; they then perfonned the procedure so they 
could use the mask in case of failure to intubate. Therapists 
were also instructed that if, after initial attempts, intubation 
could not be achieved, they should persist with bag-and-mask 
support pending the arrival of the anesthesiologist. We believed 
this would allow the therapists to fall back on a skill with which 
they were generally comfortable and would minimize the risk 
of traumatizing the airway and creating a situation where the 
anesthesiologist would be unable to intubate. 

Results 

Our results over the first 1 8 months are presented in Fig- 
ure 2. Of the nonarrest cases, 65 of 75 had an anesthesiolo- 
gist present. An anesthesiologist supervised 39 of 89 cardiac 
arrest intubations. Of the 104 supervised intubations, super- 
vised either because of daytime hours or because they were 
urgent rather than emergent, all were successfully intubated. 
Anesthesiologist were not initially present for 60 intubations; 
and, of these, 2 were never intubated and both patients died. 
Three patients were intubated by a surgeon who was present 
after an initial attempt by a respiratory therapist was not suc- 
cessful, and one patient was supported with a bag and mask 
after initial unsuccessful attempts by a respiratory therapist 
and a surgeon, at which time tlie on-call anesthesiologist arrived 
and intubated the patient. This resulted in 54 successful unsu- 
pervised intubations by respiratory tlierapists. The unsuccessful 
intubations were in patients with difficult airways — one had 
massive facial swelling and the other was in a halo follow- 
ing transoral cervical spine surgery. Neither patient had been 



164 Out-of-operating-room intubations 



74 Nonarrest cases 




39 Anesthesloiogist 

present 

(ali intubated) 



10 Emergent 

(no anesthesiologist, 

all intubated) 



50 No anesthesiologist 



40 Successful intubations 



Fig. 2. Results of the 164 consecutive out-of-operating-room intu- 
bations performed during the first 18 months, using this model. 



expected to survive; and upon their arrival the anesthesiol- 
ogists were also unable to intubate either patient. Our model 
resulted in 162 of 164 patients successfully intubated. 

Discussion 

This retrospective 1 8-month review of our inuibation model 
demonstrates that an airway management algorithm used in 
a tertiary care medical center does not necessarily require an 
in-house anesthesiologist or emergency physician. The 1 .2% 
failure rate is within reported rates for out-of-operating-room. 
intubations (Table 2).'"'' Meaningful statistical comparisons 
with other reports are difficult because of variations in the 
patient populations described, the circumstances described, 
and definitions of complications and failure rates. Some reports 
include only out-of-hospital intubation while others are lim- 
ited to intensive care unit intubations only. Other reports do 
not note a failure rate but include intubations taking longer 
than 10 minutes or requiring extensive attempts. Our train- 
ing discouraged repeated attempts by the therapist, substituting 
bag-and-mask support until the anesthesiologist arrived and 
established a plan. Table 2 summarizes existing studies and 
the circumstances and outcomes described. The low inci- 
dence of complications and the variation in definitions makes 
statistical comparison to other models virtually impossible. 
Rather, we judged our results to be acceptable based on out- 
come and based on failure rates within the range described 



554 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



TWO-TIERED RESPONSE FOR EMERGENCY AIRWAY MANAGEMENT 



Table 2. Reported Results for Out-of-Operating-Room Intubations 



Author 


Inlubators 


Setting 


Experience 
(% failure) 


Mascia'" 


Anesthesiologists 


In-hospital 


13/613 failed (2) 


McLaughlin 


Therapists 


In-hospital 


50/50 intubated. 


& Scott" 






but 10% required 
longer than 5 min 


Conley & Smith' 


Therapists 


In-hospital 


3/74 failed (4) 




Anesthesiologists 




0/30 failed 




Certified nurse 




0/5 failed 




anesthetists 








Other physician 




4/34 failed (121 


Schwartz etal" 


Critical care 


Intensive care 


0/297, Unrequired 




physician 


unit 


> 4 attempts, 2 
required 10 attempts 


Thalmanet al'- 


Therapists 


In-hospital 


42/833(5) 


Zyla& Carlson" 


Therapists 


In-hospital 


18/178(10) 


Stauffer et al" 


House physician 


In-hospital 


1/97 failed (1), 




or anesthesiologist 




20% required > 4 
attempts 


Stewart et aH 


Paramedics 


Field cardiac 
arrest 


70/779 (8) 


DeLeo'-" 


Paramedics 


Field 


74/785 failed (9) 



ther. we had observed that the more complex airway prob- 
lems (requiring anesthesiologist involvement) were in patients 
who were deteriorating but had not yet arrested. Patients 
requiring emergent intubation generally had already suf- 
fered cardiac arrest. Following cardiac arrest, there is no 
need to consider the issues of sedation, muscle relaxation, 
or hemodynamic instability with intubation. One prior study 
of emergency room intubations found that 9 of 22 intuba- 
tions for respiratory failure required prolonged attempts ver- 
sus only 3 of 2 1 in patients who had suffered cardiac arrest,'^ 
corroborating our experience that intubations for cardiac arrest 
tended to be less complicated. 

The impetus for establishing this program was the loss of 
an anesthesia resident position. To continue in-house cov- 
erage by a physician skilled in airway management would 
have required an additional 12 hours per weekday night of 
physician time to cover a 6 pm-6 am shift plus 48 hours per 
weekend, for a total of 5,628 additional hours of coverage. 
The cost for an anesthesiologist or emergency physician in 
our area was $50-75/h. We also considered the possibility 
of a nurse anesthetist but at a cost of $40/h, the additional 
expense would have been formidable. We thus estimated a 
cost of well over $200,000/yr to provide emergency airway 
coverage during night and weekend hours. The costs of our 
training program were minimal, and we expect the costs for 
recertification each year to remain low. Given the excellent 
initial outcomes, the program seems both clinically effec- 
tive and cost-effective. 



from other institutions. To perform a study demonstrating that 
this model was better would require numbers of patients that 
would be impossible to achieve. 

Given the difficulty with statistical comparisons, we 
reviewed each case to consider whether we believed the out- 
come would have been different under our prior system of 
24-hour in-house anesthesiologist presence. Under this model 
for 57% of the intubations, an anesthesiologist was still pre- 
sent, and in no case could we identify any morbidity from 
a delay in intubation pending the arrival of an anesthesiol- 
ogist. /Vmong the remaining intubations, the airway was gen- 
erally established promptly by the respiratory therapist. In 
three cases a surgeon intervened after an initial failed laryn- 
goscopy by a therapist. The surgeons had all completed anes- 
thesia rotations and the interventions took place while the 
airway was controlled and before the therapists had begun 
to pursue alternative strategies. The two patients who were 
never intubated did not have a change in their expected out- 
comes because both were judged to have terminal illnesses 
prior to their arrests. 

This model was established based on prior experience at 
our institution. We had noted that the majority of intubations 
actually occurred in patients who exhibited signs of pro- 
gressive deterioration over a period longer than 30 min. Fur- 



Conclusions 

Although a recent survey found that only 1 % of hospitals 
with anesthesiology training programs had respiratory ther- 
apists perform out-of-operating-room intubations, our model 
establishes that involving therapists in intubations can be cost- 
effective and provide an excellent level of care. 



REFERENCES 



Nayyar P, Lisbon A. Non-operating room emergency airway man- 
agement and endotracheal intubation practices: a survey of anes- 
thesiology program directors. Anesth Analg 1997;85( 1 ):62-68. 
National Board for Respiratory Care CRTT and registry exam con- 
tent outlines. Lenexa KS: National Board for Respiratory Care; 1997. 
Membership Directory. Association of Anesthesia Program Direc- 
tors. Park Ridge IL: Association of Anesthesia Program Directors; 
October 1997. 

Stewart RD. Paris PM. Winter PM, Pelton GH, Cannon GM. Field 
endotracheal intubation by paramedical personnel: success rates and 
complications. Chest 1984;85(3):341-345. 
Conley JM, Smith DJ. Emergency endotracheal intubation by res- 
piratory care personnel in a community hospital. Respir Care 
1981;26(4):336-338. 



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555 



TWO-TIERED RESPONSE FOR EMERGENCY AIRWAY MANAGEMENT 



6. McLaughlin AJ Jr. Scott W. Training and evaluation of respiratory 
therapist in emergency intubation. Respir Care 1 98 1 ;26(4):333-335. 

7. Downs JB. Who should intubate? (editorial). Respir Care 
l981;26(4);331-332. 

8. Taryle DA, Chandler JE, Gixxl JT Jr., Potts DE, Sahn SA. Emergency 
room intubations-complications and survival. Chest 1979;75(5):541- 
543. 

9. Stauffer JL, Olson DE. Petty TL. Complications and consequences 
of endotracheal intubation and tracheotomy: a prospective study of 
1 50 critically ill adult patients. Am J Med 198l;70(l):65-76. 

1 0. Ma.scia MS, Matijasko MJ. Emergency airway management by anes- 
thesiologists (abstract). Anesthesiology I993;79:1054. 



Schwartz DE, Malthay MA, Cohen NH. Death and other complications 
of emergency aiiway management in critically ill adults. A prospec- 
tive investigation of 297 tracheal intubations. Anesthesiology 
1995;82(2):367-376. 

Thalman JJ, Rinaldo-Gallo S. Maclntyre NR. Analysis of an endo- 
tracheal intubation service provided by respiratory care practition- 
ers. Respir Care 1993;38(5):469-473. 

Zyla EL, Carlson J. Respiratory care practitioners as secondary 
providers of endotracheal intubation: one hospital's experience. Respir 
Care I994;39(l ):30-33. 

DeLeo BC. Endotracheal intubation by rescue squad personnel. Heart 
Lung 1977;6(5):851-854. 



556 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Acute Pulmonary Effects of Toxic Nitrogen Dioxide Fume Inhalation 

Dheeraj Gupta MD DM, Ashutosh Nath Aggarwal MD DM, Sanjayjain MD DM, 
Digamber Behera MD, and Surinder Kumar Jindal MD 



OBJECTIVES: To study pulmonary function in subjects accidentally exposed to nitrogen diox- 
ide fumes. DESIGN: Case series. SETTING: Medical emergency service and respiratory lab- 
oratory at a tertiary care hospital in North India. PARTICIPANTS: Sixty-three male workers 
exposed to toxic fumes following an accidental explosion in a tunnel at their workplace. MEA- 
SUREMENTS & RESULTS: Six severely ill subjects were hospitalized; of them, 2 patients with 
acute respiratory distress syndrome needed assisted ventilation, one of whom died. Spirome- 
try performed on the other 57 mildly affected subjects revealed restrictive defect in 42 (74%) 
and obstructive defect in 2 (4% ) subjects. Arterial blood gas ( ABG) analysis showed hypoxemia 
in 9 (16% ) and respiratory alkalosis in 34 (60% ) of these subjects. CONCLUSIONS: Acute toxic 
exposure to nitrogen dioxide fumes is potentially fatal. Even mildly affected and asymptomatic 
individuals may show abnormalities on pulmonary function evaluation. [Respir Caie 1998;43(7):557- 
56 1 ] Key words: Pulmonaiy function, nitrogen dioxide, toxic exposure, arterial blood gases, spirom- 
etiy. acute inhalation injun: 



Introduction 

Concern about the toxicity of the oxides of nitrogen has 
been frequently expressed in clinical and toxicological literature. 
TTie earliest evidence of human toxicity was recorded in 1 804 
when a merchant and his dog died after breathing nitric acid 
fumes.' Since then, occupational exposures to the oxides of 
nitrogen as a by-product in the process of silage fermenta- 
tion, with acetylene oxygen flame in the field of welding, by 
improper detonation of explosives in mining activities, and. 
rarely, as a complication during anesthesia in medicine have 
been recorded.- '' 

Of all the oxides of nitrogen, nitrogen dioxide is proba- 
bly responsible for most of the pulmonary effects. Molecu- 
lar nitrogen and oxygen combine to form nitric oxide (NO) 



Dheeraj Gupta MD DM. Ashutosh Nath Aggarwal MD DM. Digamber 
Behera MD. and Surinder Kumar Jindal MD, Department of Pulmonary 
Medicine; and Sanjay Jain MD DM. Department of Internal Medicine, 
Postgraduate Institute of Medical Education and Research, Chandigarh, 
India. 

Reprints & Correspondence: Dr S K Jindal. Head. Department of Pul- 
monary Medicine, Postgraduate Institute of Medical Education and 
Research. Chandigarh 160012 (India); e-mail: skjindal@chl.vsnl.net. in. 



if heated to more than 2000° C. By cooling to approximately 
600° C, nitrogen dioxide (NO2) forms, which is a heavy red- 
brown pungent gas.'* Workers engaged in mining or under- 
ground tunnel activities are exposed to these gases either after 
the use of explosives or from diesel exhaust. Long-term expo- 
sures may lead to chronic lung damage characterized by hyper- 
inflation.^ Massive exposure over a shoil period of time may 
result in acute lung toxicity, especially with exposures in excess 
of 200 parts per million (ppm).^" 

A few investigators have studied pulmonary function in 
volunteers exposed to low levels of NQt (around 4 ppm or 
less) under controlled experimental conditions.'"'"" Some data 
are also available regarding pulmonary function in hospitalized 
patients who presented with acute lung toxicity.^ '"•'* We 
recently evaluated pulmonary function in a group of work- 
ers engaged in underground tunnel activities. The subjects were 
referred to us for respiratory assessment shortly after expo- 
sure to toxic fumes following an accidental explosion in a car- 
riage carrying explosives. 

Subjects & Methods 

Sixty-three workers from an upcoming hydro-electric power 
project located more than 250 kilometers from this institute 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



557 



Acute Pulmonary Effects of Toxic Nitrogen Dioxide Fume Inhalation 



in the neighboring state of Himachal Pradesh were referred 
following exposure to toxic fumes after an accidental explo- 
sion in an underground tunnel. All of the subjects were work- 
ing in the underground tunnel at the time of explosion. We 
saw the affected individuals approximately 48 hours after the 
mishap occurred. We obtained a detailed history regarding 
symptoms and smoking habits from all subjects and performed 
relevant physical examinations. We admitted severely affected 
patients for indoor management and followed them until dis- 
charge or death. We gave only symptomatic therapy to the 
remainder and observed them for up to 24 hours before they 
were discharged home. 

After obtaining informed consent, we performed spirom- 
etry on all subjects capable of performing pulmonary func- 
tion tests, using a Morgan Spiroflow spirometer (P K Mor- 
gan Ltd. Kent UK). We recorded forced vital capacity (WC), 
forced expiratory volume in the first second (FEV|). and peak 
expiratory flow (PEF) for all subjects as per standard guide- 
lines, and expressed results at body temperature and pressure 
saturated with water vapor (BTPS)." We calculated the pre- 
dicted normal values for different parameters using regres- 
sion equations previously derived by us.-" We also expressed 
FVC, FEVi and PEF recordings as a percentage of normal 
predicted values (FVC%, FEVi%, and PEF%. respectively). 
We interpreted spirometric data using FVC, FEV], and 
FEVi/FVC ratios as the primary variables.-' We defined restric- 
tive defect as FVC < 80% of predicted with a normal 
FEVj/FVC ratio, and obstructive defect as an FEV|/FVC ratio 
< 70%. We classified severity of restriction (or obstruction) 
as mild for FVC (or FEV|) between 61-80%. moderate for 
41-60%. and severe for < 40% of the predicted values. Esti- 
mation of total lung capacity (TLC) and lung compliance could 
not be carried out due to logistic reasons; hence, these vari- 
ables were not included for the confirmafion of restrictive 
defects identified on spirometry. 

We obtained blood samples from the radial artery using 
a heparinized syringe, with the subject breathing room air (or 
supplemental oxygen in severely affected individuals) for arte- 
rial blood gas (ABG) analysis. We defined normoxemia as 
P02 > 80 mm Hg [10.6 kPa] and hypoxemia as Pq, 60-79 mm 
Hg [8.0 - 10.5 kPa] (mild): Pq, 45-59 mm Hg [6.0-7.9 kPa] 
(moderate); and Pq: < 45 mm Hg [6.0 kPa] (severe).-- We 
defined normocapnia as Pco: 35-45 mm Hg [4.7 - 6.0 kPa], 
hypocapnia as Pco: less than this range, and hypercapnia as 
more than this range. We defined normal pH as 7.35 to 7.45. 

Results 

All the subjects seen in the Emergency Service were men 
with a mean age of 28.4 (± 6.9) years (range 20-53 yrs). Fifty- 
two of the 63 subjects (83%) were asymptomatic; others com- 
plained of dyspnea, chest discomfort, burning in eyes, gid- 
diness, vomiting, and headache. Two had severe respiratory 
distress, altered sensorium, and bilateral crepitations on aus- 



cultation. ABG analysis showed severe hypoxemia, and their 
chest radiographs revealed bilateral extensive alveolar infil- 
trates. Neither had any known pre-existing cardiac disease; 
however, pulmonary capillary wedge pressure measurements 
were not available. Considering these findings, we diagnosed 
acute respiratory distress syndrome ( ARDS) in both the patients 
in accordance with standard criteria.-' Four more patients had 
severe dyspnea and/or chest discomfort. We admitted these 
6 patients and discharged the remaining 57 subjects after obser- 
vation and symptomatic treatment. The 2 patients with ARDS 
required assisted ventilation, one of whom had refractory 
hypoxemia and died within 1 2 hours of admission. The sec- 
ond pafient improved after 7 days of mechanical ventilation. 
The other 4 severely affected patients improved with sup- 
plemental oxygen therapy and were discharged after 2 (3 
patients) or 3 days ( 1 patient). These 6 patients had moder- 
ate to severe hypoxemia on room air at the time of admission 
(Table 1 ). 

Table 1. Clinical Details of 6 Severely Affected Subjects 



Subject, ABG at Admission 

Age (Room Air) 

(years) Pq, Pcoj 

(mm Hg) (mm Hg) 



Chest Radiograph* 



1,26 


21 


39 


Bilateral alveolar 

infiltrates suggestive 

of ARDS' 


Ventilated 
& recovered 


2,26 


32 


34 


Bilateral alveolar 

infiltrates suggestive 

of ARDS 


Ventilated 
but died 


3.37 


52 


28 


Normal 


Recovered 


4,24 


56 


28 


Normal 


Recovered 


5, 30 


52 


32 


Normal 


Recovered 


6.24 


37 


35 


Normal 


Recovered 



* Chest radiographs of the other 57 mildly affected individuals were normal 
t ARDS = acute respiratory distress syndrome 



Table 2. Classification of Spirometry Data in 57 Mildly Affected Subjects 



Number of subjects 


18 


39 


57 


Normal study 


3 


10 


13(23) 


Mild obstruction 


1 


1 


2(3) 


Mild restriction 


10 


22 


32 (56) 


Mixlerate restriction 


4 


5 


9(16) 


Severe restriction 





1 


1(2) 



558 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Acute Pulmonary Effects of Toxic Nitrogen Dioxide Fume Inhalation 



a 



M 



&-a"&*>i>*5>'5-<&'5'<&'S--i>-i-<g>'S"%'& ^-fe,- 



FVC (% of Predicted) 

Fig 1 . Distribution of forced vital capacity (FVC) (expressed as a per- 
centage of normal predicted) in 57 mildly affected subjects. 



Study of ABG analyses and spirometry performed on the 
57 less severely affected subjects showed interesting findings 
(Tables 2 & 3). Spirometry revealed a restrictive defect in most 
of the subjects (Table 2 & Fig. 1). Of the 2 subjects with 
obstructive defects, one had an FEVi/FVC ratio of 68% with 
an FEV| value of 63% of predicted; the other had an 
FEV|/FVC ratio of 65% with an FEVi value of 61% of pre- 
dicted. Only one of them was a smoker, with a 7 pack-year 
smoking history. The only subject with severe restriction, 
revealed with spirometry, had mild hypoxemia and did not 



complain of any symptoms. The presence or severity of restric- 
tion on spirometry was not associated with any particular symp- 
tomatology or the degree of hypoxemia on ABG analysis. Chest 
radiographs done in all subjects with abnonnalities on spirom- 
etry and/or ABG analysis were within normal limits. 

We compared the variables studied in the mildly affected 
individuals between the smoking and nonsmoking subjects. 
There were 18 (32%) smokers of 1 to 40 pack-years. Although 
FEV|%, FVC%, and PEF% were all lower among smokers 
in comparison to nonsmokers, the differences were not sta- 
tistically significant (Table 3). Only the FEVi/FVC ratio was 
significantly reduced in smokers (p < 0.05). Diagnoses obtained 
on analyzing spirometry data were also not significantly dif- 
ferent for the two groups (Table 2). 

ABG analysis showed mild hypoxemia in 6 ( 1 1 %) and mod- 
erate hypoxemia in 3 (5%) subjects; Pco: was normal in 23 
(40%) and low in 34 (60%) subjects; the latter group was diag- 
nosed to have respiratory alkalosis. pH was normal in 48 (84%) 
and alkalotic in 9 ( 16%) subjects. 

Among the mildly affected subjects, we did not find any 
significant difference in the ABG values or spirometry data 
between the symptomatic and asymptomatic subjects. 

On follow-up, the patient who had recovered after 
mechanical ventilation was completely asymptomatic and 
had normal spirometry. Further evaluation for estimation 
of lung compliance or TLC was therefore not done. Other 
subjects have not reported for subsequent follow-up despite 
repeated reminders to the concerned authorities, presumably 
because the laborers in such projects usually consist of migrant 
population. 



Table 3 Pulmonary Functions in 57 Mildly Affected Smoker and Nonsmoker Subjects (Mean, Standard Deviation, and 95% Confidence Intervals) 



Nonsmoker (n = 39) 



Smoker (n =18) 



Total (n = 57) 



FEV|.*L 

FEV|, % of predicted 

FVC.L 

FVC, % of predicted 

FEV|/FVC.%t 

PEE, L/min 

PEE, % of predicted 

Po;, mm Hg 

Pco;. mm Hg 

pH 



2.76 ±0.70 (2.55 -2.97) 

82 ±19(76-88) 

2.97 ±0.81 (2.72-3.22) 

73 ±17 (67 -78) 

94 ± 6 (92 - 96) 

442 ±105(409-475) 

93 ±20 (86- 100) 
84.7 ±15.0(79.3-90.1) 
33.9 + 3.5(32.6-35.2) 
7.42 ± 0.03 (7.40 - 7.44) 



2.52 ±0.53 (2.28 -2.76) 
76 ±16 (68 -84) 

2.80 ±0.52 (2.28 -2.76) 

70 ±13(64-76) 

90 ±7 (86 -93) 

395 ±90 (314 -476) 

85 ±18(77-93) 

82.6 ±9.4 (76. 1 -89.1) 
33.8 ±3.0 (33.7 -35.9) 

7.40 ±0.05 (7.36 -7.44) 



2.69 ±0.66 (2.5 1-2.87) 

80± 18(75-85) 

2.91 ±0.73(2.71 -3.01) 

72 ±16(68-76) 

93 ±7 (91 -95) 

427+102(401-454) 

91+20(86-96) 
85.3 ± 14.3 (80.8 - 89.8) 
33.8 ±3.3 (32.8 -34.8) 
7.42 ±0.04 (7.40 -7.441 



* FEV| = forced expiratory volume in tfie first second ; FVC = forced vital capacity ; FEV|/F^C = ratio of forced expiratory volume in ttie first second to forced 
vital capacity; PEF = peak expiratory flow. 
' p < 0.05 



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559 



Acute Pulmonary Effects of Toxic Nitrogen Dioxide Fume Inhalation 



Discussion 

Acute toxic pneumonitis following an exposure to high 
doses ofNOi may present as acute respiratory distress syn- 
drome shortly after exposure.'' progressive breathlessness — 
which is generally related to an obliterative bronchiolitis-'* — 
starting a week or two after exposure, or a combination of the 
two. NO: reacts with water in the respiratory tract to fomi nitric 
acid, which then dissociates into nitrates and nitrites.-' These 
substances damage the cells of the respiratory tract by var- 
ious mechanisms such as direct toxic damage, peroxidation 
of cell membrane lipids by free oxygen radicals.-" inhibition 
of surfactant.-' and collagen degradation.-** Methemoglobinemia 
may also conUnbute to hypoxia.'' Because of its low solubility. 
NO: causes damage deep in the respiratory tract at the level 
of conducting airways and adjacent respiratory bronchioles, 
resulting in a noncardiogenic pulmonary edema. Patients usu- 
ally present with cough (dry or productive), wheeze, dysp- 
nea, central chest pain, sweating, and weakness a few hours 
after exposure.- -' Examination may reveal fever, tachypnea, 
wheeze, and/or hypotension in severely affected individuals. 
Although mildly affected patients usually improve with sup- 
portive treatment and supplemental oxygen, severely affected 
cases may need mechanical ventilation. 

Acute respiratory distress syndrome is a well-recognized 
complication of acute NO: exposure, and exposed patients 
usually require mechanical ventilation during the time the lung 
injury recovers. Despite timely intervention, the damage may 
still prove fatal. It is well known that both the concentration 
of the gas and the exposure time dictate the severity of dam- 
age.'* Incidentally, we did not have the actual levels of the toxic 
gases in the environment at the time of the accident. It was. 
therefore, not possible to quantify the severity of exposure 
in the cases reported. 

The available data on pulmonary functions following acute 
severe exposure to NO: fumes is sparse. Most of this infor- 
mation is limited to severely ill patients requiring hospital- 
ization, in whom both restrictive and obstructive defects have 
been identified.'* ""* Reduction in the diffusing capacity and 
compliance of the lung have also been noted.'^ '' Ailerial blood 
gas analysis shows varying degrees of hypoxemia and res- 
piratory alkalosis, with a widened alveolo-arterial gradient, 
even in less severely affected individuals.- ''^"'^ Experiments 
have also been conducted on healthy volunteers breathing low 
concentrations of NO: (up to 4 ppm) under controlled con- 
ditions for varying lengths of time. Most of these studies have 
not shown any statistically significant alteration in pulmoniu^ 
functions.'" '■* 

Our results indicate that both restrictive and obstructive 
defects may be seen in mildly affected individuals. Previous 
investigators have reported obstmctive defects during the acute 
phase following severe exposures and often in nonsmokers 
and patients with no other underlying pulmonary disease.^ '** 
Obsti-uctive defects and increase in airway resistance have been 



demonstrated in a few studies on subjects exposed to low lev- 
els of NO: under controlled conditions. ''* Obstructive defects 
in our study were ob.served even in nonsmokers and light smok- 
ers, implying that the results were probably independent of 
the smoking habit. However, the majority of patients had 
restrictive defects on spirometry. This could be attributed to 
a possible subclinical alveolitis that was reflected in the spirom- 
etry results. Estimation of TLC. or lung compliance, was, how- 
ever, not carried out for the confirmation of these findings. 
Although the final diagnosis of a restrictive lung abnormal- 
ity is based on reduction in TLC. vital capacity may be used 
to suspect and assess severity of restriction in situations where 
TLC measurements are not available.-' Vital capacity mea- 
surements correlate well, though not absolutely, with TLC. 

Except for 3 subjects, all other mildly affected subjects 
(95%) were able to maintain adequate oxygenation (Pq: > 60 
mm Hg) on room air. We. therefore, believe that the damage 
at the alveolar level, if any. was little and not important enough 
to impair gas exchange. The hypocapnia and respiratory alka- 
losis may result from tachypnea and hyperventilation related 
to this damage. 

There were no significant differences in the ABG and 
spirometry results between symptomatic and asymptomatic 
individuals. It is possible that the symptomatic individuals 
did not have a more severe exposure. These differences were 
probably only related to individual differences in symptom 
perception (only 5 of 57 subjects were symptomatic and the 
only subject with a severe restrictive defect on spirometry was 
asymptomatic). 

A proportion of patients with severe exposure may have 
residual lung damage, mainly in the form of obliterative bron- 
chiolitis, even after complete recovery from the acute event.-"* 
In the absence of adequate follow-up data, we cannot at this 
time predict if some of these subjects will ultimately develop 
a similar complication. 

Conclusion 

In summary, we have studied 63 patients accidentally 
exposed to NO: fumes. One patient of the 6 severely affected 
died. In some of the remaining 57 less affected individuals, 
we could demonstrate abnormalities on spirometry and ABG 
analysis, possibly due to subclinical damage to the lungs. 

REFERENCES 

1 . Ramirez RJ, The first death from nitrogen dioxide fumes: the story 
of a man and his dog. JAMA i974;2:9(9):1181-l!82. 

2. Douglas WW. Hepper NGG. Colby TV. Silo-filleris disea.se. Mayo 
Clin Proc 1989;64(.'();291-.W4. 

.^. Norwood WD, Wiseh;irt DE, E;irl CA, Adley FE. Anderson DE. Nitro- 
gen dioxide poisoning due to melal-eutting with oxyacetylene torch. 
J Occup Med l96(i;S((il:.^lll-,^06. 

4. Muller B. Nitrogen dioxide intoxication after a mining accident. Res- 
piration 1969;26{4):249-261, 



560 



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Acute Pulmonary Effects of Toxic Nitrogen Dioxide Fume Inhalation 



5. Powell M. Toxic fumes from shotfiring in coal mines. Ann Occup 
Hyg 1%1;3:I62-183. 

6. Clutton-Brock J. Two cases of poisoning by contamination of nitrous 
oxide with higher oxides of nitrogen during anaesthesia. Br J Anaesth 
1967;39(5):3SS-.^92. 

7. Kennedy MCS. Nitrous fumes and coal-miners with emphysema. Ann 
Occup Hyg 1972;15(2):285-301. 

8. Lowry T. Schuman LM. Silo filleris disease: a syndrome caused by 
nitrogen dioxide. JAMA 1956;126:153-160. 

9. Lillinglon GA. Nitrogen dioxide - the new lyellow perili. JAMA 
1970;212(8):I368. 

1 0. Linn WS. Solomon JC, Trim SC, Spier CE, Shamoo DA. Venet TO. 
et al. Effects of exposure to 4 ppm nitrogen dioxide in healthy and 
asthmatic volunteers. Arch Environ Health 1985;40(4):234-239. 

1 1 . Hackney JD, Thiede FC, Linn WS. Pedersen EE. Spier CE. Uw DC, 
Fischer DA. Experimental studies on human health effects of air pol- 
lutants. Part IV. Short-term physiological and clinical effects of nitro- 
gen dioxide exposure. Arch Environ Health 1978:33(4): 176- 180. 

1 2. Kerr HD. Kulle TJ. Mcllhany ML. Swidersky P. Effects of nitrogen 
dioxide on pulmonary function in human subjects: an environmental 
chamber study. Environ Res 1979;19(2):392-404. 

13. Mohsenin V. Airway responses to 2.0 ppm nitrogen dioxide in nor- 
mal subjects. Arch Environ Health 1988;43(3):242-246. 

1 4. Worid health Organization. Environmental Health Criteria 1 88: Nitro- 
gen oxides (2nd edition). Geneva: Worid Health Organization, 1997. 

15. Scott EG. Hunt WB Jr. Silo filleris disease. Chest 1973;63(5):701- 
706. 

1 6. Moskowitz RL. Lyoas HA. Cottle HR. Silo filleris disease: clinical, phys- 
iologic and pathologic study of a patient. Am J Med 1964:36:457-462. 

1 7. Horvath EP. doPico GA. Barbee RA. Dickie HA. Nitrogen dioxide- 



induced pulmonary disease: five new cases and a review of the lit- 
erature. J Occup Med 1978;20(2):103-1 10. 

1 8. Jones GR. Proudfoot AT. Hall JI. Pulmonary effects of acute expo- 
sure to nitrous fumes. Thorax 1973;28( 1 ):6I-65. 

19. American Thoracic Society. Standardization of spirometry. 1994 
update. Am J Respir Crit Care Med 1995; 152(3): 1 107-1 136. 

20. Jindal SK. Wahi PL. Pulmonary function laboratory in the tropics: 
needs, problems and solutions. In: Sharnia OP. editor. Lung disease 
in the tropics. New York: Marcel Dekker; 1991:523-542. 

21 . American Thoracic Society. Lung function testing: selection of ref- 
erence values and interpretation strategies. Am Rev Respir Dis 
199l;144(5):1202-1218. 

22. Malley WJ. Clinical blood gases: applications and noninvasive alter- 
natives. Philadelphia: Saunders; 1990. 

23. Bernard GR. Artigas A, Brigham KL, Cadet J. Faike K. Hudson L. 
and the Consensus Committee. The American- European Consen- 
sus Conference on ARDS: definitions, mechanisms, relevant outcomes, 
and clinical trial coordination. Am J Respir Crit Care Med 1 994: 1 49( 3 
Part 1):8 18-824. 

24. Wright JL. Inhalational lung injury causing bronchiolitis (review). 
Clin Chest Med l993;14(4):635-644. 

25. Ainslie G. Inhalational injuries produced by smoke and niu-ogen diox- 
ide (review). Respir Med 1993;87(3):169-174. 

26. Thomas HV. Mueller PK. Lyman RL. Lipoperoxidation of lung lipids 
in rats exposed to nitrogen dioxide. Science 1968; 159(8 14):532-534. 

27. Dowell AR. Kilbum KH, Pratt PC. Short-term exposure to nitrogen 
dioxide: eft'ects on pulmonary ultrastructure. compliance, and the sur- 
factant system. Arch Intern Med 1 97 1 ; 1 28( 1 ):74-80. 

28. Hatton DV. Leach CS. Nicogossian AE. Collagen breakdown and 
nitrogen dioxide inhalation. Arch Environ Health 1977;32(l):33-36. 



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561 



Case Reports 



Intractable Wheezing Due to an Obstructing Tracheal Neuroendocrine 
Tumor in an Adolescent with HIV Infection 

Shari Eason Ludlam RRT MPH, David Zeldman RRT, Lauren V Wood MD, 
and Frederick P Ognibene MD 



We describe a 13-year-old boy with human immunodeficiency virus (HIV) infection who pre- 
sented with wheezing, fever, and dyspnea. Because he had a history of wheezing with a previ- 
ous episode of viral pneumonia, he underwent diagnostic procedures for possible pulmonary 
infections and was treated for exacerbation of reactive airway disease. When he failed to respond 
to aggressive anti-inflammatory and bronchodilator therapy, further workup revealed an endo- 
bronchial neuroendocrine tumor occluding 75% of the trachea at the level of the carina. We 
describe our patient's treatment and review the literature on endobronchial lesions in HIV-infected 
patients. [RespirCare 1998;43(7):562-566] Key words: Human immunodeficiency virus, bronchial 
obstruction, reactive airways disease, endobronchial neuroendocrine tumor, pediatrics. 



Introduction 

The relationship between wheezing, airflow obstruction, 
and human immunodeficiency virus (HIV) infection is unclear. 
The published literature includes studies that found an asso- 
ciation between HIV infection and evidence of wheezing or 
airflow obstruction' ' and studies where no increased frequency 
of wheezing was found in this population.^ Both reactive air- 
way disease and airflow obstruction from endobronchial lesions 
of the airways have been described. 

In immunodeficient children, reactive airway disease is 
felt to be common.' It is postulated that frequent or recurrent 
infection may induce inflammation, resulting in aii"way hyper- 
responsiveness. It is also possible that altered immunity and 
circulating immunoglobulins contribute to airflow limitations. 
Ellaurie and colleagues'' noted that approximately 30% of 



Shari Eason Ludlam RRT MPH, David Zeidman RRT. Lauren V Wood 
MD, and Frederii;l< P Ognibene MD. Critical Care Medicine Department 
of the Warren G Magnuson Clinical Center of the National Institutes of 
Health and the HIV/AIDS Malignancy Branch of the Division of Clinical 
Sciences of the National Cancer Institute, Bethesda, Maryland. 

Reprints & Correspondence: Frederick P Ognibene MD, Critical Care 
Medicine Department, Building 10, Room 7D4.1, 10 Center Drive, MSC 
1662, National Institutes of Health, Bethesda MD 20892-1662. 



infants and children with HIV infection develop wheezing at 
some point during the course of their disease, particularly with 
episodes of Pneumocystis carinii pneumonia or lymphocytic 
interstitial pneumonitis. 

We describe a case of severe wheezing and dyspnea in an 
adolescent with HIV infection that was due to airway obstruc- 
tion caused by an undifferentiated neuroendocrine tumor. We 
also review the literature describing endobronchial lesions in 
HIV-infected patients. 

Case Summary 

A 13-year-old boy with transfusion-related acquired immun- 
odeficiency syndrome (AIDS), Mycobacterium avium-intra- 
cellulare infection, and failure to thrive presented with wheez- 
ing, respiratory distress, and fever. He had a history of mild 
asthma following a viral pneumonia three years prior, that was 
treated with aerosolized albuterol sulfate for about one month. 
Until the onset of acute symptoms, the patient had not required 
any additional asthma therapy. 

The patient was admitted to the hospital and Ueated for reac- 
tive airway disease with albuterol sulfate, hydration, intra- 
venous (I.V.) methylprednisolone, and I,V. antibiotics. He 
responded to this treatment and was discharged within five 
days. Sputum was negative for P. carinii. respiratory syncytial 



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Intractable Wheezing Due to an Obstructing Tracheal Neuroendocrine Tumor 



virus, and other viral pathogens. Pulmonary function testing 
revealed severe obstructive disease with forced expiratory vol- 
ume in the first second (FEVi) 27'7r of predicted, FEV|/forced 
vital capacity ratio of 29%, reduced lung volumes and dif- 
fusion capacity, and no response to bronchodilators, despite 
the clinical improvement observed. 

The patient continued to improve until 1 3 days after dis- 
charge, when he presented with wheezing and emesis. Symp- 
toms persisted despite emergency room treatment, and he was 
transferred to our critical care unit. 

Physical examination upon admission revealed a thin male 
adolescent in moderate respiratory distress with prolonged 
expiration, suprasternal and intercostal retractions, and inter- 
mittent wheezing. The patient was afebrile. Chest radiograph 
demonstrated lung hyperinflation but no infiltrates. Direct laryn- 
goscopy revealed chronic oral candidiasis but was otherwise 
unremarkable. 

After three days of aggressive therapy in the intensive care 
unit with I.V. and aerosolized bronchodilators and high dose 
I. V. corticosteroids, blood gas analysis no longer showed evi- 
dence of hypercarbia. However, the patient continued with 
intermittent periods of severe respiratory distress with wheez- 
ing, retractions, and nasal flaring. 

Given the lack of clinical improvement, despite intensive 
treatment for reactive airway disease, diagnostic options were 
considered. However, the patient suddenly complained of 
severe dyspnea, developed hypercarbia, and required urgent 
endotracheal intubation. After intubation the patient's wheez- 
ing resolved. Subglottic stenosis was observed during laryn- 
goscopy for the intubation, and the etiology of the patient's 
wheezing was presumed to be mechanical obstruction rather 
than bronchospasm. 

Computerized tomography (CT) of the chest and neck was 



obtained (Fig. I ). Approximately 1 .5 cm above the carina, a 
12-mm polypoid mass was obstructing about 75% of the tra- 
chea. Patchy infiltrates were noted in the upper lobes, while 
the left lower lobe was completely collapsed. 

The patient underwent rigid bronchoscopy and laser exci- 
sion of the mass. Follow-up CT revealed residual tracheal nar- 
rowing of about 10%, resolved left lower lobe collapse, and 
a small amount of persistent atelectasis. Preliminary histopatho- 
logic assessment revealed superficial fungal elements. A final 
pathological diagnosis was not made due to tissue necrosis 
from the laser. The patient was discharged with the plan to 
closely follow the mass with serial CT and magnetic resonance 
imaging. Over the subsequent six weeks, the mass increased 
in size and repeat laser excision via bronchoscopy was required 
for tissue diagnosis. The final histopathologic diagnosis based 
on a chromogranin stain was an undift'erentiated neuroendocrine 
tumor (Fig. 2). A total of 4l80cGy radiotherapy was admin- 
istered over five days and, in conjunction with the laser exci- 
sion, resulted in a considerable increase in the tracheal lumen, 
although some residual mass remained (Fig. 3). 

Discussion 

Neuroendocrine tumors are a diverse group of malignancies, 
such as small-cell lung carcinoma, neuroblastoma, and car- 
cinoid tumors, that share common structural features upon 
examination with light microscopy.^ Although similar in com- 
position, clinically these tumors grow and respond to ther- 
apy very differently. The incidence of this tumor is unknown; 
in fact, Lequaglie and colleagues'* at the National Cancer Insti- 
tute of Milan reported that neuroendocrine carcinoma of the 
lung may be misdiagnosed or unrecognized. In 10 years of 
experience with 1 9 patients at this center, surgery was cura- 




Fig. 1. Computerized tomography of the chest of the 13-year-old boy, revealing an intratracheal mass lesion (arrow) obstructing 
approximately 75% of the tracheal lumen. 



Respiratory Care • July 1998 vol 43 No 7 



563 



INTRACTABLE WHEEZING DUE TO AN OBSTRUCTING TRACHEAL NEUROENDOCRINE TUMOR 



tive for more than half of the patients with locahzed disease. 
Some patients were treated with adjuvant chemotherapy, 
based on analysis of their tumors. Tumors recurred in 10 of 
the 19 patients, with seven of these metastases occurring in 
the brain. Although surgery and chemotherapy are rec- 
ommended for this tumor, our patient was so clinically and 
nutritionally debilitated, that his oncology team did not 
recommend chemotherapy. Surgery was similarly ruled out 
because of the same clinical concerns and the questionable 
benefit of further tumor reduction. Radiation was therefore 
given as palliative therapy. Six months following comple- 
tion of radiation therapy, this patient developed metastatic 
recurrence of his disease that was treated successfully with 
chemotherapy. 

Endobronchial lesions are an uncommon pulmonary com- 
plication of HIV infection.** '" Because patients can present 
with symptoms mimicking other, more frequently occurring, 
pulmonary complications of HIV infection, it is important for 
the respiratory care clinician to be aware of them. The most 
common endobronchial lesion associated with HIV infection 
is Kaposi sarcoma (KS). 

KS is an AIDS-defining illness." It typically presents with 
pink or red lesions of the skin or mucous membranes. The exact 
frequency of pulmonary KS is not known, although it is esti- 
mated to affect 8-14% of HIV-infected patients with respi- 
ratory symptoms, and up to 49% of HIV-infected patients with 
mucocutaneous KS.'-" In pediatric patients with HIV infec- 
tion. KS is rare.^ Although pulmonary KS in the absence of 
skin, mucous membrane, or lymphoid lesions has been reported, 
it typically occurs in the setting of widespread disease. Typ- 
ical symptoms of pulmonary KS include cough and dyspnea, 
making it potentially difficult to distinguish from other pul- 




Fig. 2. A. Photomicrograph of the tracheal mass using the 
AE1/AE3 monoclonal antibodies stain forcytokeratin demonstrates 
evidence of epithelial carcinoma (20\ x 10. 200-fold magnifica- 
tion). B. Photomicrograph of the tracheal mass using the chromo- 
granin stain demonstrates reactive uptake of granules characteris- 
tic of neuroendocrine tumors (20x x 10, 200-fold magnification). 




Fig. 3. Computerized tomography of the chest of the 13-year-old boy after laser excision of the mass and five weeks of radiother- 
apy. Arrow indicates residual intratracheal mass. 



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monary manifestations of HIV infection. Furthermore, up to 
half of patients with pulmonary KS can have concurrent infec- 
tions.'"* Airway obstruction due to compression of the upper 
or lower airways can occur, resulting in wheezing or stridor. 
The prognosis of pulmonary KS is poor, and treatment with 
chemotherapy or radiation is palliative. 

Both Mycobacterium tiiherciilosis'^'^ and atypical Mycobac- 
terium species''^'-' with endobronchial manifestations have been 
reported to occur in up to 18-25% of HIV-infected patients 
with tuberculosis. Fever, cough, and dyspnea are common 
presenting symptoms. Clinically significant airflow obstruc- 
tion can develop, either from compression of the airway by 
the endobronchial mass or swollen lymph nodes or possibly 
from a hypersensitivity reaction to relea.sed tubercular anti- 
gens during antituberculosis therapy.-- Treatment of the hyper- 
sensitivity reaction with corticosteroids has been successful. 
Endobronchial mycobacterial infections usually respond to typ- 
ical antituberculosis therapy, albeit slowly. Residual airway 
stenosis can persist after resolution of the disease. 

Endobronchial non-Hodgkin"s lymphoma has been doc- 
umented in two case reports.-'-"* The exact incidence of tho- 
racic involvement with non-Hodgkin"s lymphoma is unknown, 
but it is thought to be rare, usually less than 10% of the HIV- 
infected patients who have non-Hodgkin"s lymphoma.-"* How- 
ever, the incidence of non-Hodgkin"s lymphoma is thought 
to be increasing among HIV-infected patients, so endobronchial 
lymphomas may be seen more frequently in the future. Patients 
with endobronchial non-Hodgkin's lymphoma typically pre- 
sent with severe dyspnea, dysphagia, or wheezing. The prog- 
nosis of endobronchial lymphoma is poor, and treatment with 
chemotherapy or radiation therapy is palliative in nature. 

Adenocarcinoma of the lung is another cause of endo- 
bronchial lesions. There is no strong evidence that HIV- 
infected individuals have an increased incidence of lung car- 
cinoma compared to HIV seronegative patients. However, 
some clinicians have noticed an altered clinical presentation 
in HIV-infected patients, including younger age at diagno- 
sis, more advanced disease stage at presentation, and short- 
ened survival.-'"-' 

Pulmonary aspergillosis,-* bacillai7 angiomatosis,-'' bac- 
terial and cytomegalovirus tracheitis,'" actinomycosis,-'" 
Rlwdococcus equi,^' Pneumocystis carinii,^- pediatric smooth 
muscle tumors," Nocardia asteroides?* and granular cell 
myoblastoma'"" have also been noted to be rare causes of endo- 
bronchial lesions in some HIV-infected patients. The small 
number of reported patients with these atypical endobronchial 
lesions precludes generalizations about their association with 
HIV infection or their prognoses. However, many of the 
reported patients died within a short time of diagnosis. The 
patients with bacterial tracheitis and nocardiosis responded 
to therapy and survived to hospital discharge. The reported 
cases of smooth muscle tumor, bacillary angiomatosis, endo- 
bronchial P. carina, pulmonary actinomycosis, and two of 
four cases of Aspergillus tracheobronchitis all failed to respond 



to therapy and subsequently died. Outcomes of endobronchial 
Rliodococcus equi were not reported. 

Our patient's clinical course is instructive. First, final 
histopathologic diagnosis revealed a very unusual etiology 
of an endobronchial lesion in an HIV-infected patient. The 
incidence of maligmuicy in children with HIV infection is much 
less than that for adults. Lymphomas and leiomyosarcomas 
are the two most frequently reported pediatric malignancies 
associated with HIV infection."' Another interesting feature 
of our patient's illness was his initial improvement in clin- 
ical symptoms following his first hospitalization for reactive 
airway disease, despite his lack of response to bronchodila- 
tors on pulmonary functions tests. The role that corticosteroids 
played in his recovery from this first episode is unclear. His 
improvement, coupled with his history of asthma led to delay 
in correct diagnosis and definitive therapy. Finally, unlike many 
other HIV-infected patients with endobronchial lesions, our 
patient had a good outcome, despite his metastatic recurrence. 
As noted, his metastases responded to cheinotherapy, and he 
remains alive and functioning well. 

Conclusion 

In summary, we have presented a case of life-threatening 
airway obstruction caused by a neuroendocrine tumor in an 
adolescent with HIV infection. To our knowledge, this is a 
previously undescribed phenomenon. Although rare, health 
care providers should consider the possibility of endobronchial 
lesions as a cause of airflow obstruction in HIV-infected 
patients, particularly if there is no improvement with bron- 
chodilator and anti-intlammatory therapy. 

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Kemper CA, Hosteller JS, Follansbee SE, Ruane P, Covington D, 
Leong SS, et al. Ulcerative and plaque-like tracheobronchitis due to 
infection with Aspergillus in patients with AIDS (review). Clin Infect 
Dis 1993;17(3):344-352. 

Slater LN. Min KW. Polypoid endobronchial lesions: a manifesta- 
tion of bacillary angiomatosis. Chest 1992;102(3):972-974. 
Cendan I, KlaphoLz A, Talavera W. Pulmonary actinomycosis. A cause 
of endobronchial disease in a patient with AIDS. Chest 
1993;103(6):1886-1887. 

Canfrere I, Germaud P, Roger C, Another cause of endobronchial 
lesions found in HIV patients (letter). Chest 1995;108(2):587-588. 
Gagliardi AJ, Stover DE. Zaman MK. Endobronchial Pneumocys- 
tis carinii infection in a patient with the acquired immune deficiency 
syndrome. Chest 1987;9l(3):463-464. 

Balsam D. Segal S. Two smooth muscle tumors in the airway of an 
HIV-infected child. Pediatr Radiol 1992;22(7):552-553. 
Pickles RW. Malcolm JA. Sutherland DC. Endobronchial nocardiosis 
in a patient with AIDS. Med J Aust l994;l6l(8):498-499. 
Ganti S. Marino W. Granular cell myoblastoma in an HIV positive 
patient. N Y State J Med 1991;91{6):265-266. 
McClain KL. Joshi VV, Murphy SB. Cancers in children with HIV 
infection (review). Hematol Oncol Chn North Am 1996; 10(5): 1 189- 
1201. 



566 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



A Tribute To John H Emerson 



Jack Emerson: Notes on His Life and 
Contributions to Respiratory Care 



Richard D Branson RRT 



If you have had the pleasure of attending the annual meet- 
ing anytime in the last couple of decades, you undoubtedly 
caught a glimpse of a tall, aristocratic figure hovering around 
the Emerson booth. That distinctive. New England. Ichabod 
Crane-like frame belonged to John Haven Emerson (Fig. 1 ). 
Better known as "Jack," Emerson was a pioneer in biomed- 
ical device development, with a particular emphasis on res- 
piratory equipment. His death in February 1997 at the age of 
91 brought to close a remarkable, storied, yet surprisingly quiet 
career in ingenious innovation. 

Emerson was bom February 5, 1906, in New York City 
to a scholarly family. He was educated in private schools. As 
a youngster he attended the Ethical Culture School and grad- 
uated despite lacking a few of the required studies. His son 
George remembers that Jack would often quip. "I never grad- 
uated from high school." Attending an Ivy League school was 
a tradition for Emerson children. Jack's father. Haven Emer- 
son, was a Professor of Public Health at Columbia Univer- 
sity in New York. In fact, I came across a manuscript by Haven 
Emerson, regarding artificial respiration for resuscitation.* 
Apparently the apple did not fall far from the tree. Jack, how- 
ever, was not interested in a higher education and preferred 
to tinker and attempt to solve problems with the materials ready 
at hand. 



Richard D Branson RRT. Department of Surgery, University of Cincin- 
nati Medical Center, Cincinnati, Oliio. Mr Branson is an Associate Editor 

of Respiratory Care. 

Reprints & Correspondence: Richard D Branson RRT. Department of 
Surgery. University of Cincinnati Medical Center. PO Box 670558. 231 
Bethesda Ave— Room 2457, Cincinnati OH 45267-0558: e-mail: bran- 
sord@uc.edu. 

*Emerson HA. Artificial respiration in the treatment of edema of the 
lungs: a suggestion based on animal experimentation. Arch Intern 
Med 1909:3:368-371. Reprinted on Pages 583-584 in this issue, with 
permission. 



Despite protests from his family, at the age of 22, Emer- 
son purchased the rudiments of a machine shop from the estate 
of a local inventor. His father refused to aid in this folly, but 
his mother arranged for the $ 1 ,600 necessary for the purchase. 
He moved this equipment to a small warehouse at 15 Brat- 
tle Street in Harvard Square and set up shop. There Emerson 
built research apparatus to order for professors and researchers 
at the prestigious schools of medicine and physiology in the 




Fig. 1. John Haven Jack" Emerson, February 5, 1906 
February 4, 1997 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



567 



Jack Emerson: Notes on His Life and Contributions to Respiratory Care 



Boston aiea. It is interesting that many of his early clients were 
relatives who had more closely followed the Emerson fam- 
ily traditions. 

In 1928 Emerson designed a Barcroft- Warburg apparatus 
for tissue respiration studies. These devices were used for stud- 
ies of photosynthesis and in later years for cancer research. Essen- 
tially, this device used tissue cultures in small flasks that were 
agitated in a constant temperature waterbath. Gases generated 
during growth were measured in U-shaped manometers. 

Emerson designed, in 1930, a micromanipulator for the 
precise movement of instruments under a microscope. This 
device proved invaluable in early physiology research includ- 
ing cell manipulation and injection. Decades later the same 
device would find use in the assembly of electronic parts. Emer- 
son designed this device for his older brother Robert, who was 
a faculty member of the Botany Department at Harvard. 

In 1931 Emerson built an oxygen tent that included an 
improved system for cooling the patient's environment. Antibi- 
otic therapy was not yet available and oxygen therapy was 
the mainstay of treatment. Previous devices were prone to rust 
and failure. 

Emerson is best known for the development of the iron lung 
during the polio epidemic of the 1930s. According to David 
Garrison (one of Jack's relatives and a co-worker), Emerson's 
father, then Health Commissioner of New York City, began 
to notice the escalating number of polio cases. Haven took his 
son aside and suggested, "If you are ever going to make an arti- 
ficial respirator, now is the time." Evidently, the two had pre- 
viously discussed the possibility, unbeknown to others. 

At the time Drinker was the leading manufacturer of iron 
lungs, but Emerson's improvements to the design were clas- 
sic examples of his work to come — simple, functional, and 
cost effective. The Drinker iron lung was developed by Philip 
Drinker, Louis Agassiz Shaw, and James Wilson at Harvard. 
Upon hearing of Emerson's dalliance into making respirators. 
Drinker warned Jack that he owned the patents on these devices 
and to expect litigation if Emerson continued to pursue this 
technology. What followed represents the spirit of Jack Emer- 
son, perhaps as well as any other event. He ignored Drinker's 
warning and went about producing iron lungs that were qui- 
eter, more reliable, and cheaper than Drinker's. When the law- 
suit arrived, Emerson and his colleagues began an exhaus- 
tive search of the engineering and medical literature from 
Europe and the United States. The result of that research is 
contained in a bright yellow pamphlet' available from the J 
H Emerson Company, containing photographs and drawings 
of negative pressure ventilation devices preceding Drinker's 
by decades. Drinker's patents were declared invalid, for want 
of an invention. The resourcefulness of Emerson and com- 
pany produced prior ailwork that proved that although Drinker 
may have had some excellent ideas, others had them earlier. 

The Emerson design replaced blowers and valves with a 
flexible diaphragm. The flexible diaphragm was fashioned 
from elk hide in a dual layer. In this fashion, if one layer became 



torn, the second redundant layer would continue operation. 
Emerson also improved the shape and size of the chamber by 
having it manufactured by a boiler company in Boston (Mar- 
ket Forge). The result was a quieter, simpler, lighter, and less 
expensive device. Although difficult to source, the Emerson 
device was said to cost half the price of the Drinker device. 
Emerson's first device was used for a polio patient at Chapin 
Hospital in Providence, Rhode Island. The patient had been 
given last rites, but survived the illness. This iron lung, affec- 
tionately referred to as "Old No. 1 ," now resides in the Smith- 
sonian Institution. Emerson's improvements to the iron lung 
continued, and he added a quick opening and closing func- 
tion, an improved pressure gauge, and emergency hand oper- 
ation. Emerson's design was innovative and yet so simple, 
it was copied by others. His final development of the iron lung 
was the creation of a transparent positive pressure dome to 
allow ventilation when the body compartment was opened 
for patient care. 

Like other ventilator entrepreneurs of his time (Foirest Bird 
and V Ray Bennett), Emerson was involved in the develop- 
ment of demand valves for high altitude flight and SCUBA 
(self-contained underwater breathing apparatus) for the Navy. 
In 1942 Emerson developed an automatic resuscitator, which 
provided alternating positive and negative pressure along with 
delivering oxygen. His interest in resuscitation techniques led 
to his formulation of the Emerson method of artificial res- 
piration for drowning victims. This technique placed the patient 
in the prone position and alternately raised and lowered the 
patient's hips. The hipbones were grasped and lifted upward 
to create inspiration and drainage of fluid out of the lungs. 
When the hips were lowered, exhalation occurred. This method 
was widely used, replacing the Shafer prone pressure tech- 
nique, until the introduction of mouth-to-mouth resuscitation. 

In 1949 Emerson turned his attention to positive pressure 
devices and created a mechanical assistor for anesthesia. Using 
the bag-in-the-box technique, Emerson's device was triggered 
by patient effort, and the ventilator compressed the bag, ven- 
tilating the patient. This device was developed in concert with 
the anesthesia depailment at Harvard. 

Emerson developed equipment for intennittent positive pres- 
sure breathing (IPPB), cardiopulmonary bypass equipment, 
hospital beds, negative pressure ventilators (pneumo-wrap), 
and body positioning devices. In 1955 Emerson introduced 
a pleural suction pump that provided continuous low-pres- 
sure suction for thoracostomy tubes in postoperative thoracic 
surgery. These devices were on wheels, utilized a large glass 
jar and a quiet, effective pump. These devices continue to be 
widely used and are well known as Emerson Postop Pumps 
in surgery departments around the world. 

In 1957 Emerson built a volume plethysmograph for Dr 
Jere Mead at Massachusetts General Hospital for the mea- 
surement of residual lung volume. Mead was a preeminent 
pulmonary physiologist of his time. This device was later 
adapted for the measurement of other lung volumes. At Mead's 



568 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



JACK EMERSON: NOTES ON HIS LIFE AND CONTRIBUTIONS TO RESPIRATORY CARE 



encouragement, Emerson also developed the first "deep breath" 
modification for negative pressure ventilation, a predecessor 
of the sigh breath. Mead"s idea was first suggested by Viss- 
cher. who believed a periodic deep breath would restore lung 
compliance. 

In 1964 Emerson built one of the early volume ventilators. 
This simple device resembled a green washing machine and 
used a piston to deliver precise volumes. Oxygen was added 
into a "trombone-shaped" accumulator connected to the intake 
of the piston for delivery of elevated Fio- The tidal volume 
was changed by a crank on the front of the inachine. which 
controlled the stroke of the piston. Respiratory rate and inspi- 
ratory-to-expiratory-time ratio (I:E) were adjustable. The 
humidifier was a modified pressure cooker and was known 
as the Emerson Hot Pot. A belt, connected to a DC motor and 
pulley wheel, served to move the piston. In case of failure of 
the existing belt, a spare was hung inside each cabinet. The 
belts were similar to those used to circulate air in forced air 
gas furnaces in homes. On numerous occasions I have heard 
the story of the belt becoming loose or breaking and the spare 
found to be missing. Under these circumstances, the resource- 
ful respiratory therapist would run to the parking lot and obtain 
the belt from a Volkswagen Beetle (the old one) and place 
it in the Emerson to restore it to working order. Eve never 
looked to see whether the two belt sizes are compatible because 
it's such a good story. In any event, the Emerson Postop Vol- 
ume Ventilator was reliable and would allow ventilation of 
patients when other devices failed. Emerson's device was not 
the first of the piston ventilators (Morch and Engstrom pre- 
ceded him), but it was the first device to allow independent 
control of I:E. 

Eorthe intermittent mechanical ventilation (IMV) Emer- 
son used continuous flow IMV and a unique water column 
PEEP (positive end-expiratory pressure) valve to allow suc- 
cessful use of IMV and a very low work of breathing. Dur- 
ing the introduction of microprocessor ventilators with demand 
valves, numerous investigators compaied the work of breath- 
ing of the new devices to the "Emerson" gold standard. In fact, 
the IMV champions of the 1970s were all great supporters 
of Emerson ventilators, because the work of breathing was 
low and the possibility of successful application of the tech- 
nique maximized. 

In 1954 Emerson was intrigued with the idea of a dog's 
ability to ventilate normally during panting. He developed a 
device for "vibrating' the patient's airway. His patent- for this 
device. No. 2,918,917: Apparatus for Vibrating Portions of 
a Patient's Airway, issued in 1959 made several unique obser- 
vations. 

This invention pertains to an apparatus for treat- 
ing a patient by vibrating a column of gas which 
is in communication with his airway at a rate which 
is greater than the patients normal rate — from 1 (X) 
to 1 ,500 vibrations per minute — vibrating the col- 



umn of gas doubtless causes the gas to diffuse more 
rapidly within the airway and therefore aiding in 
breathing function by circulating the gas more thor- 
oughly to and from the walls of the lungs. 

The initial device used a reciprocating diaphragm, simi- 
lar to the high-frequency oscillation devices used today. A 
continuous flow of air was provided from a blower and directed 
into the inspiratory circuit. The diaphragm was connected to 
a shaft, which was attached to a pulley. A second electric motor 
turned the pulley by means of a belt. As the pulley turned, the 
shaft "vibrated' the diaphragm. In the 1970s Emerson exper- 
imented with a series of high-frequency devices, settling on 
a device that did not incorporate a diaphragm. The final high 
frequency device was simple and functional. A high-pressure 
gas source was delivered to a rotating ball. The ball had a hole 
drilled through the center to allow the passage of gas into the 
patient circuit. The faster the ball would spin, the higher the 
frequency. As the spinning speed was reduced, volume through 
the hole and duration of tlow {% inspiratory time) increased. 
This device is frequently referred to as a High-Frequency Flow 
Interrupter (HEED, owing to the mechanical design (Fig. 2). 



Flowmeter 
(0.75 LPMl 



Air-Oxygen 
Blender 








Reservoir Tank 



DC IVlotor 



,^C 



BBBB 



.Motor Speed Control 




— Constant 
Flow In 



■ Interrupted Flow Out 
Detail of Bali Valve 



Fig. 2. Schematic of the Emerson High-Frequency Flow Interrupter 
used for high-frequency positive pressure ventilation. 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



569 



Jack Emerson: notes on his life and Contributions to Respiratory Care 



Several authors reported successful use of this device in the 
1980s.'-' 

Throughout his lifetime, Emerson had long-standing rela- 
tionships with the leaders in respiratory care, critical care, 
surgery, anesthesia, and pulmonary medicine. Alvin Barach 
was a close Emerson colleague and was instrumental in devel- 
opment of the "In-Exsufflator Cough Machine," a device gain- 
ing new acceptance now as a method of secretion removal 
in patients with neuromuscular disease. Many of you may rec- 
ognize this device by its earlier name, the name given it upon 
its initial introduction, "The Cofflator." The Cofflator was 
Barach's invention and, despite his influence, never really 
caught on with clinicians. The In-Exsufflator improved on 
the idea and provided the flows required to aid in secretion 
removal. Emerson also developed Barach's walking cane, 
which contained 50 L of oxygen in an unobtrusive hollow cane. 

I was introduced to Jack Emerson by Forrest Bird and 
enjoyed many conversations with Mr Emerson over the past 
decade. Despite his advancing age, Emerson was always 
patient and willing to discuss any matter of interest. He would 
always surprise me by reaching into his worn briefcase and 
pulling out an original manuscript or conference proceeding 
from the 1940s or 1950s. These would often have his hand- 
written notes and those of others (Barach, Mead, and others) 
in the margin. He would often produce this as evidence that 
all the new techniques we were talking about at the meeting 
had been done many times before. In the last years of his life, 
he would frequently lament over the state of relations between 
the government, clinicians, and manufacturers. He would pro- 
duce the 1 955 proceedings'* on the state-of-the-art conference 
on negative pressure ventilation and suggest that cooperation 
between the groups was a key to early success in mechani- 
cal ventilation. Emerson liked to reminisce about the days when 
a physician could call for a needed piece of equipment, and 
he could create the device in a couple of days and bring it in 
for a patient trial. In fact, the very first Emerson iron lung was 
never tested on anyone but Jack Emerson himself, before going 
on a patient. Perhaps this could be considered an Emerson inno- 
vation as well, true quality control. 

This issue of RESPIRATORY CARE contains several pieces 
as a tribute to the life of a man who saved and changed the 
lives of others. I did not know Mr Emerson well, but he usu- 
ally remembered my name and was always congenial and 
enlightening. The respect he garnered from Forrest Bird — 
who called him Jack, but always answered his questions with 
'sir' — provided me some insight into the magnitude of his 
stature. A lot can be learned about a person by observing the 
respect shown them by leaders in their field. 1 was fortunate 
enough to have a photograph taken with Jack Emerson and 
Forrest Bird during the American Association for Respira- 
tory Care meeting in Las Vegas in 1994 (Fig. 3); an enlarged 
version graces the wall of my office. 

I do not know how Mr Emerson would have felt about this 
issue of the Journal. He was quiet and self-effacing. He didn't 




Fig. 3. From left: John Haven Emerson, Richard D Branson RRT, 
and Forrest M Bird during the 1994 American Association for Respi- 
ratory Care annual meeting in Las Vegas. 



seem to care much for attention or honors. He was like his 
devices — simple, functional, and reliable. The role Jack Emer- 
son has played in the history of biomedical engineering has touched 
the lives of hundreds of thousands of people on both sides of his 
equipment. His entrepreneurial spirit and simple, innovative genius 
will be sorely missed in this microprocessor world. 

ACKNOWLEDGMENT 

This piece could not have been written without the kind 
cooperation and assistance of George Emerson. I am grate- 
ful for his honesty and hope that this issue of the Journal will 
invoke fond memories of his father. 

REFERENCES 

1 . Tlie evolution of iron lungs. Cambridge MA: J H Emerson Company; 
1978. 

2. Emerson JH, inventor; J H Emerson Company, assignee. Appara- 
tus for vibrating portions of a patient's airway; U.S. patent 2,918.917. 
I9.'i9. 

3. El-Baz N. Faber LP. Doolas A. Combined high-frequency ventila- 
tion for management of temiinal respiratory failure: a new technique. 
Anesth Analg I98.3;(i2( I ):,19-40. 

4. Frant/ ID .^rd. Werthammer J, Stark AR. High-frequency ventila- 
tion in premature infants with lung disease: adequate gas exchange 



570 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Jack Emerson: Notes on His Life and Contributions to Respiratory Care 



al low tracheal pressure. Pediatrics 1983;7i(4);48_V488. 

5. Gettinger A, Glass DD. High-frequency positive pressure ventilation 
pressure. Use in neonatal and adult intensive care. In: Carlon GC, How- 
land WS, editors. High-frequency ventilation in intensive care and 
during surgery. New York: Marcel Dekker Inc; 1985:63-75. 

6. Blum-Hoffmann E, Kopotic RJ. Mannino FL. High-frequency oscil- 
latory ventilation combined with intermittent mandatory ventilation 
in critically ill neonate: three years of experience. Eur J Pediatr 
1988;l47(4l:392-398. 

7. Kopotic RJ. Mannino FL, Boynton BR. A system for high-frequency 
oscillatory ventilation and intermittent mandatory ventilation in 
neonates. Crit Care Med 1986; 14(71:642-645. 

8. Minutes of the round table conference on polymyelitis equipment. 
May 28-29, 1955; New York. 

ADDITIONAL READING & GENERAL BIBLIOGRAPHY 

Bach JR. Mechanical insufflation-exsufflation. Comparison of peak expi- 
ratory flows with manually assisted and unassisted coughing tech- 



niques. Chest I993;I04(5):I553-I562. 

Bach JR. Update and perspective on noninvasive respiratory muscle aids. 
Part 2: The expiratory aids (review). Chest 1994;105:1538-1544. 

Beck GJ, Barach AL. Value of mechanical aids in the management of 
apatient with poliomyelitis. Ann Intern Med 1954;40:1081-1094. 

Beck GJ, Scarrone LA. Physiological effects of exsufflation with neg- 
ative pressure (EWNP). Dis Chest 1956;29;1-16. 

Emerson J. Respiratory problems in poliomyelitis. National Foundation 
for Infantile Paralysis Conference, Ann Arbor MI. March 1952; 1 1 . 

Ferris BG, Mead J, Whittcnherger JL, Saxton GA. Pulmonary function 
in convalescent poliomyelitis patients. III. Compliance of the lungs 
and thorax. New Engl J Med 1952;247:390-397. 

Garrison DL. J H Emerson and his company (unpublished). 

Visscher MB. The physiology of respiration and respirators with par- 
ticular reference to poliomyelitis. National Foundation for Infantile 
Paralysis Round Table Conference. Minneapolis MN. October 
1947:156. 

Williams EK. Holaday DA. The use of exsufflation with negative pres- 
sure in postoperative patients. Am J Surg 1955;90:637-640 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



571 



— Foreword — 
Some Reflections on the Man Behind the Machines 



From its origins in applying bellows to resuscitate drown- 
ing victims in the 1760s, the field of mechanical ventilation 
has advanced because clinical needs have been identified and 
then met by clever inventors and engineers, whose technical 
and engineering expertise engendered new and better 
machines. No exception to this pattern, the history of mod- 
em mechanical ventilation has been shaped by several cre- 
ative innovators whose names are emblazoned on the equip- 
ment we commonly use today, for example, Bennett, Bird, 
Engstrom. and Emerson. 

The field lost one of these innovators this past year — John 
Haven "Jack" Emerson — and it seems fitting for RESPIRA- 
TORY Care to commemorate his career by publishing his 
own reflections on the contributions he made to the fields of 
mechanical ventilation and to respiratory care. The accom- 
panying article is a transcript of a lecture that Emerson deliv- 
ered to the Massachusetts General Hospital Department of 
Anesthesia Critical Care group in 1985. At that time, we invited 
Mr Emerson to address this group regarding these reflections. 

A few words of explanation are needed for the reader. First, 
this lecture was invited as an informal seminar, accompanied by 
a few of Emerson's selected slides (some of which are repro- 
duced as figures). The article is a transcript of a lecture and there- 
fore reflects the folksy spontaneity of conversation rather than 
the polish of a chapter-ready manuscript. Indeed, the editors 
have purposely avoided rigorous editing in order to preserve 
the folksy affability that was an endearing trait of Jack Emerson. 



Also, Mr Emerson names specific persons in his lecture 
and we have done our best to transcribe the names accurately, 
while recognizing that the 1 3-year-old recording leaves room 
for errors in this regard. Most of the names of the question- 
ers could not be deciphered. 

Finally, I would like to add a personal introductory note. 
As a Fellow in Critical Care at the Massachusetts General 
Hospital then, I had the privilege of inviting and introduc- 
ing Jack Emerson. I distinctly remember the self-effacing 
enthusiasm with which he agreed to deliver the lecture. My 
experience of inviting and hearing the lecture was framed 
by two main feelings: first, awe at meeting the man behind 
the machines that we used daily in our intensive care units 
then and second, reverence for the sense of craftsmanship 
that Jack Emerson exuded as he described a career of build- 
ing sturdy, practical, life-saving machines. Overall, I believe 
that this article will pay tribute to Jack Emerson by putting 
his own words before the readership of RESPIRATORY CARE 
and, in so doing, celebrate thoughtful innovation and crafts- 
manship — values that will surely enhance our own practices 
of respiratory care. 



James K Stoller MD 

Associate Editor 
RESPIRATORY CARE 



James K Stoller MD, Department of Pulmonary and Critical Care 
Medicine, Head. Section of Respiratory Therapy, Cleveland Clinic Foun- 
dation. Cleveland Ohio. At the time of the lecture transcribed on the fol- 
lowing pages, Dr Stoller was a fellow in Critical Care at Ma.s.sachusetts 
General Hospital, Boston. Massachusetts. 



572 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Some Reflections on Iron Lungs and Other Inventions 

John H Emerson 



Transcribed from the videotaped lecture given by Mr Emerson during a meeting oftlie Department of 
Anesthesia Critical Care at Massachusetts General Hospital in 1985. 



Thank you very much for asking me. I hope I can tell you 
some things you'll be interested in. Now, particularly. 1 gather 
you'd like to know how our ventilator came about. If I put 
these slides through, I might put them through right in the 
beginning, quickly — ^just so you can see how I got started. 

I was from New York, and I didn't do very well in school 
at all. I never graduated from high school. My family sent 
me up here, because everybody went to Harvard or Radcliffe. 
That was traditional in my family. In fact, my father told me 
if I didn't go. I'd be the first Emerson since they landed on 
the shores of Ipswich — but that's me! My brother, who was 
in plant physiology at Harvard, got me a job in the physics 
lab. 1 swept floors and learned how to oil lathes and machine 
stuff. 

Then next year I got a job at the medical school trying 
to make very, very fine fibers for a cousin of mine, Alexan- 
der Forbes, for a string galvanometer. He was trying to make 
one-centimeter-long fibers, gold plated, of quartz for a gal- 
vanometer, a special galvanometer he was having made, 
studying nerve action currents, which they were not able to 
study in those days, because the galvanometers wouldn't 
respond fast enough. So. if you had it short and small, and 
they wanted a half a p — you know how big that is — you look 
at a .spider web, and then you reduce it. You could hardly see 
these darned things! And I found a way to make them for him. 
Took me about a year, and they used to blow quartz in a room 
that was all covered with felt, and they'd pick them up off the 
wall, these little things. I had a bunch of things that spun around 
like that, and I wound them up. 

Anyway. I decided then that. well, my brother being a plant 
physiologist, studied chlorophyll — what do they call it? — pho- 
tosynthesis was his specialty, and he was trying to get pure 
cultures, and I developed a micromanipulator for him to get 
pure cultures, which is still on the market. In fact, there was 
a guy came to my shop very recently. He'd gone all over 
Europe, went to Zeiss and Leitz and came back here and some- 



body said, why don't you come over to our place? And he 
bought the manipulator that I had made for my brother. It's 
different in that instead of having things that go that way and 
that way, to move that way and that way, I had a lever like 
an airplane control — no matter which way you moved the han- 
dle, it moved the needle that you were controlling, very lit- 
tle, in the opposite direction. It reversed it. so under a micro- 
scope, it was erected. This has been a useful instrument for 
people. In fact, talking about nerve action currents, it was used, 
a bunch of them together, at Boston University, way back then 
for tracing the fibers out of a cat's brain to find out what con- 
trolled what. See. that's the kind of thing they were doing in 
those days, and they used my manipulator. 

Anyway. let's go quickly through this, and then I'll tell you. 
There's the oxygen tent I told you about, which I made for 
James Wilson. He was a resident at Children's Hospital. Let's 
see now, it was probably '29 or so that I made that. He had 
a milk pail that he bought at Sears Roebuck. There was a brand 
new Sears Roebuck store, that one that's over there. He used 
the milk pail and put a motor under it. The trouble was that — 
you put ice in that thing — and the motor was underneath to 
circulate the air to the tent. Only trouble was they were made 
of 'tinned' steel and in a very short time the salt and ice rusted 
the steel tank out that dripped on the motor, and it wasn't a 
good arrangement. So, we made one out of copper for him, 
and he wanted something that wasn't as cumbersome as 
Barach's tent for pediatrics. 

OK, let's just go quickly. All right, here's the iron lung. 
Now. the same Jim Wilson, (I've just got to go a little into 
how I got into this) Jim Wilson then asked me if I had any 
ideas on how to improve the Drinker respirator (Fig. I ). That 
was a new thing, and they were selling them for around $3,600. 
It was a rectangular tank affair with thick walls, because they 
were flat walls. TTiey had valves, a motor to drive valves, and 
a blower to change the pressures. So that it made an awful 
lot of noise. 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



573 



Some Reflections on Iron Lungs and Other Inventions 




Fig. 1 . The first "iron lung" to receive widespread use was developed in 1 928 in Boston, and was patented by Philip Drinker and Dr Louis Agas- 
siz Shaw. It was cumbersome and inconvenient but saved a number of lives. It had a sliding bed with head-wall attached, and a rubber collar. 
Pressure changes were created by a rotary blower and an alternating valve. During a polio epidemic the Consolidated Gas Company of New 
York paid for building large numbers of these respirators, and reports of their use spread quickly around the world. Reprinted, with permission 
of JH Emerson Co. 



I told him I thought that a simple diaphragm would be bet- 
ter. I made a box that size, which I took to Children's Hos- 
pital recently to show them. 1 still have the box — a very sim- 
ple thing with a big piece of leather [from] a car seat that I 
got from my junkyard. That's still in good condition, inci- 
dentally. You push the handle up and down and it would 
change the pressure in the box. Well. I took this thing over 
to Children's, and I gave it to Jim Wilson, and he said, "Could 
I keep it and take it to Drinker?" And Drinker said. "That won't 
work. We thought of that." And so they gave it back to me. 

Well, I talked to my father about this ... (this was in '30- 
'31), and about maybe a month after, I got a short letter from 
my father. Now my father was the head of public health at 
Columbia. He simply said (he was an epidemiologist) and he 
said. "We're heading for a bad epidemic of polio this year. 
If you're ever going to try that idea of yours, now's the time 
to do it." 

Well, the epidemic came pretty fast and so I went across 
the river here [to) Robertson Boiler Works, and I said (I had 
no drawings, absolutely nothing), I just went into that place 
and said, "Oh, make me a round tank about so big, well, 28 
inches, maybe, in diameter, and put some legs on it. We'll take 
it from there." After I picked that tank up, in two weeks we 
had this thing completed (Fig. 2). That machine, I got into it 
and got a bad cold (I mean a sore throat) from one night. It 
worked, you see! I took [the tank] down and showed it for 
my father at Willard Parker and one other hospital, and he told 
me to stop at Rhode Island on the way back, at their conta- 



gious hospital. I put it in there late in the afternoon and they 
told me, "Well, we have a patient. We have no machines." 
They had four Drinkers in use. You couldn't hear yourself 
think in the place it was so noisy. [The patient] was a young 
priest. They said, "He'll die at night. We have no way to ... 
we have no place to ... " We tried — so, we put the patient in — 
it worked perfectly. It ran for six months. The patient lived, 
and we decided we'd try and make iron lungs. 

I asked the Boiler Works to make five more tanks. News 
got around here in Boston that I was doing this. And I decided 
that I would try to show it at the American Hospital show, 
which was coming up in Toronto. So, I had a call from Drinker. 
No! He came into my shop and told me if I tried to make this 
iron lung he'd put me out of business. He had patents com- 
ing up. Well, in those days, you know, doctors didn't patent 
things much (and especially life-saving things). It made us 
mad, anyway, to be threatened like that. But we went ahead 
and completed the machine and took the second machine to 
Toronto. We got it coitipleted two days before the meeting, 
spent one day — no we started in the night, driving to Toronto 
with that iron lung across the back seat of a Dodge Touring 
car with the top down. As we went through Albany, it stuck 
out so far that my co-helper, Mr Garrison, was driving and 
the headrest knocked over some of these street signs. 

We made it to Toronto. We set up this booth. The Drinker 
respirator was there. We were offering [ours| at $ I, ()()(). All 
I can say is at the end of that meeting, everybody knew that 
I had the machine that was going to be used! This hospital 



574 



Respiratory Care • July 1998 Vol 43 No 7 



Some Reflections on Iron Lungs and Other Inventions 




Fig. 2. Because of a severe poliomyelitis epidemic in 1931 John Haven Emerson of Cambridge, U.S.A., built a simplified respirator. It cost less than 
half as much as others, but contained many improvements. It operated quietly, using a bellows to create the changes of pressure (as Woillez's did, 
but with a motor added). A wide range of speeds was instantly available. Opening and closing were rapid and convenient. It could be pumped by 
hand if electricity failed. The first Emerson "iron lung" is now preserved in a glass case in the United States National Museum (the Smithsonian Insti- 
tution) as the prototype of respirators constructed since 1 931 in American and Europe. Reprinted, with permission of JH Emerson Co. 



[Massachusetts General Hospital] ordered one on the spot. 
You had one of the first that I built. There was a hassle, you 
know. Harvard was mad. There was a lot of back and forth. 
Dean Edsel asked me not to advertise for six months, which 
I agreed to. And in six months, the new Drinker came out with 
all the five features that had made mine good, without my 
advertising. Anyway, we survived that, and that's just a smat- 
tering of what happened. 

So, let's go faster. That's a little one. You see how sim- 
ple it could be. Just change the pressure inside by moving that 
handle. OK. 

Now, in '36, there was an epidemic of flu, and Ralph Tra- 
bell was at Hartford. He wanted something better than the bub- 
bling bottles. So, you remember for nasal oxygen they had these 
bottles just to — they were a tube under water, they would bub- 
ble. I wanted to split the bubbles up smaller. I got two bearings — 
from a Ford generator — that are porous bronze, compressed. 
I pushed the air through that, and I got little bubbles, like that. 
That was the first of a kind of humidifier where you broke the 
bubbles up real small. That was for Ralph Trabell. OK. 

We did make one of the early IPPV [intermittent positive 
pressure ventilation] machines, too, and particularly for the 
Brigham. what was his name, [the] anesthesiologist there? 
What? Derek! Bill Derek. Bill Derek. We made an anesthesia 
machine ... a patient started to breathe, and it would assist them, 
and they tell me that it was the first with an anesthesia bag — 
you could encase or open the front of this thing and squeeze 



the bag by hand. That was in — well — later. Let's go on. 

This is the chest respirator with a cage, which I made for 
bronchoscopy, for one thing, for the Long Island College Hos- 
pital. Anyway, I guess you know pretty much about that. Next. 

This machine, you'd think maybe was an iron lung, but 
this is for Al Barach. This is one of the most sophisticated things 
we ever made. That was for treating tuberculosis, and the patient 
was completely enclosed. The Swedes developed this. A fel- 
low named Thunberg, but he just put the patients completely 
in the tank and changed the pressures up and down quite rapidly 
and got ventilation by compression and rarefaction. If you press 
here on your chest, and bring equal pressure inside, the lungs 
won't move. But you can ventilate if you get enough difference 
in pressure. This thing worked, but for closing (what do you 
call them?) the holes in the lungs, but we mu.st have made 60 
of those, and just at that time the sulfa drugs were coming, 
so that was out the window. Next. 

Oh, there's Derek's thing, see? "53 again. That's Derek him- 
self and the bag. and you could open that and squeeze the bag 
if you wanted to. It was an assisting anesthesia machine. Next. 

Incidentally, we made the first hyperbaric tank in the U.S. 
That was for Presbyterian Hospital in New York. They used 
that for a good many years. I went over to England and saw 
what they were doing over there, and then made this tank. Next. 

You all know about that. One of the chest surgeons came 
to my shop a long time ago and, well, it was way before that. 
Glover and O'Neil, that was one of the teams in Philadelphia. 



Respiratory Care • July 1998 Vol 43 No 7 



575 



Some Reflections on Iron Lungs and Other Inventions 



He said, "We're trying to expand the chest after our surgery 
with something they called a Stedman pump. I [used] 13 pumps 
and I still can't get the lungs to come up." I said, "You're doing 
it the wrong way." In two weeks or so I fixed him a little vac- 
uum cleaner affair with variable speed. We were in business 
making these things and everyone uses them. Next. 

This was for Jere Mead at the School of Public Health. His 
volume rather than the pressure plethysmograph. and a lot of 
people bought these for research. Next. 

Al Barach — he wanted oxygen for his patients. When they 
went out walking, they wanted the security of having oxy- 
gen. And he wanted a walking cane for them to ... that's a walk- 
ing cane with oxygen in it. It had 50 L in it. The FDA [Food 
and Drag Administration] didn't want it sold, because they'd 
set a rule that nothing less than 70 liters — you know, it all 
depends on — he found it useful for somebody trying to get 
up a few steps at their home. Anyway, let's go on. Next. 

There's the belt we were talking of, see, that Barach was 
using. You could cycle it. or the patient could cycle it. Next. 

This old ... would be related to the stories I'm telling you — 
(that's my wife) — and it is a good way for manual ventila- 
tion — it was a lot better than what was being used. I proposed 
the use of lifting the hips because you stretch the rib cage that 
way. You make it like a bellows, you see, instead of just push- 
ing on the back the way the Schiifer prone pressure worked, 
which was the standard way of rescue in those days. Next. 

That's the resuscitator we made. That again. Next. And 
that's the house that I traveled and sold iron lungs out of. I 
bought that on Commonwealth Avenue from [the] General 
Electric Company. They'd used it to sell kitchens. See the gen- 



erators up in front? As I drove, I'd charge batteries, and then 
I'd come into a town. I could run the iron lung that I had in 
the back, and the town would go through and see the iron lung 
they were going to spend their money for. Next. 

That's the lung now. Next. 

Now, two more. I tell you, I'm going to skip these. No. just 
go one after the other. Yeah. The last one was a French iron 
lung (Fig. 3), which saved the day in the lawsuit for us. We 
found the one at the bottom there, and here I have the actual 
picture. But the thing that saved the day was this hospital 
[Massachusetts General Hospital] forming, because you had 
a library, we came here. We found references to negative pres- 
sure cabinets from the world over! Everyone there had thought 
that Drinker was the only thing, see. And we found people 
that had this idea in many countries, a good many people in 
this country. So, this Frenchman had a real cute idea. Instead 
of a pressure gauge to tell how well he was ventilating, [he 
used] a glass tube with a rod in it, and if the chest went up 
and down, he could see how much he was ventilating. Very 
direct. Anyway. Let's go. Next. 

There's a French one (Fig. 4) — worked with a steam boiler. 
You shift the valve and it would ... and the Venturi. Next. 

Just run them through. This was in Vienna (Fig. 5). Vienna 
again. This is England (Fig. 6). All these things, now. this is 
1905 this thing was made in Tennessee (Fig. 7), Nashville. 
OK. This one and the next one were made in Massachusetts, 
or designed. OK. This was in South Africa, and the fellow 
had a patient and built on the spot an iron lung for himself 
and saved his case. Right on the spot! OK. 

This wa.s a plethysmograph that recorded. You could breathe 




Fig. 3. In 1876 Dr Woillez of Paris built the first worloble iron lung, wfiich he called a "spirophore." It had the basic elements of modern res- 
pirators, including an adjustable rubber collar and a sliding bed. A unique feature was a rod which rested lightly on the patient's chest, to 
give visual proof of actual lung expansion. In a brilliant lecture presented before the Academy of Medicine on June 20, Woillez showed a 
thorough understanding of the physiology and mechanics of artificial respiration. He refused to patent his invention. A colleague suggested 
placing spirophores all along the Seine, for drowning rescues, but finances for the public service were lacking. (This illustration was recon- 
structed by tVlaxfleld Parrish Jr for a legal battle ... .) Reprinted, with permission of JH Emerson Co. 



576 



Respiratory Care • July 1998 Vol 43 No 7 



Some reflections on Iron Lungs and Other Inventions 




Fig. 4. Dr Charles Breuillard of Paris patented a "bath cabinet" type of respirator in 1887. For a source of vacuum he recommended "a 
stream ejector fed by a steam boiler ... heated by a spirit lamp." The patient himself was supposed to operate a valve, alternately connecting 
the cabinet with the vacuum, for inhalation, and with the atmosphere, for exhalation. Breuillard also described a chest respiratory "cuirass" to 
be operated in the same, and a face mask. Reprinted, with permission of JH Emerson Co. 



dogs with it. All these were negative piiessure cabinets. Go ahead. 

This is do-it-yourself in Germany. OK. 

And that's the Drinker, you see. with the pump and stuff 
and the rectangular tank. That was what was on the market. 
Next. 

That's a room they had in Children's Hospital (Fig. 8). Five 
patients were taken at the same time. Negative pressure. OK. 

Now. we found that Alexander Graham Bell had actually 
made one that was in the museum up in Canada. I believe we 
found reports that he came down to this hospital and tested it. 
I think he used to come to this hospital. OK. I have some infor- 



mation about that. [Responding to an unintelligible comment 
from the floor.] There it is. Tlie thing to the left is what he called 
the jacket. See, it's a pot tank concealed up here and down here. 
And that's the pump. See the bellows? OK. That's it. 

I'm out of breath from ti7ing to rush. I probably shouldn't 
have tried the pictures. [Question from the floor about devel- 
opment of positive-pressure ventilators.] Well, let's see what 
I can give you on how the ventilator came about. 

I guess it's related to polio. Actually, I think around '52 
or something like that, they had an epidemic in Denmark and 
there weren't enough iron lungs. They couldn't possibly get 




^S$;^^g^^^:^^V^y;^N^^-.v.:;t^V.^-.-.:^^^;^,-'^ 




::~y-=A 



Fig. 5. In 1901 Rudolf Eisenmenger of Piski, Hungary, patented a portable respirator which consisted of a "simple, two-part box" enclosing 
only the patient's chest and abdomen. Later he became medical professor in Vienna, and there continued to improve his invention. He 
stressed the importance of access to the patient's throat and limbs, of portability, and of hand-operation. (Motors were also mentioned.) 
There are reports of "extraordinary success" with Eisenmenger's respirators. Reprinted, with permission of JH Emerson Co. 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



577 



Some Reflections on Iron Lungs and Other Inventions 





F 


C lA AS^^v^^^^^\v^-.^^^^^^^^^^^^^^ 


; 








s 


^ — . ; 








L.€^^^;£=:=i ; 



Fig. 6. William Davenport of London understood the mechanics of artificial respiration clearly. His patent in 1905 mentions a box, a rubber 
collar, and a simple bellows or piston pump. He lacked the sliding bed (of Woillez and modern iron lungs) but made several good sugges- 
tions, including the supplementary use of oxygen. He proposed several types, including a "collapsible form ... to facilitate transit." Reprinted, 
with permission of JH Emerson Co. 



enough iron lungs. Any of you heard this story? You know 
about it? They got all the anesthesia machines they could find 
in the countryside and set up students squeezing anesthesia 
bags and kept those patients going, and they survived! A lot 
of them. Their survival was as good, I guess, as the iron lung 
cases' survival, so ( I guess I'm not very polite this morning), 
but that brought a flood of anesthesiologists from Denmark 
over here. 1 think one of them is your Dr Pontoppidan. Dr Rot- 
tenberg is another one. Morch is another. I guess there were 
maybe a dozen [who] got over here to show us how they'd 
done things. 

Morch was in Chicago at the University of Chicago and 
Cook County Hospital. He made a piston inachine. As a mat- 
ter of fact, just before Morch, of course, it was the Engstrom. 
Maybe they were both around the same time, but they were 



both piston machines. They were equal cycle, in and out, and 
Don Benson worked with Morch on his machine. His, inci- 
dentally, went under the bed. Morch's was a low machine, 
about that size and so high. And the drive was horizontal, so 
the whole thing could shove under the bed where you couldn't 
see it. Then he had a tube up to the patient, and an exhala- 
tion valve, which was a big steel ball that would pop up and 
let the patient exhale. 

Anyway, Benson moved to Hopkins and he made himself 
a piston machine that he hoped would have better humidity, 
because that was one of the problems with the machine that 
Morch had made. They still weren't trying to use very high 
pressures, because everyone thought you shouldn't use pres- 
sures above, oh, 20-25 cm HiO. He had a water kettle and 
heated it. Then the gas that came out of the water kettle [passed 




Fig. 7. Dr Charles Morgan Hammond of tvlemphis, U.S.A., built his first "artificial lung" in 1905 and a series of improved models throughout 
the next 20 years. He performed experiments and treated patients successfully, but his respirators were not produced commercially and 
remained unknown to the public for many years. Reprinted, with permission of JH Emerson Co. 



578 



Respiratory Care • July 1998 Vol 43 No 7 



Some reflections on Iron Lungs and Other inventions 




Fig. 8. In the early respirators it was difficult to give complete nursing care and to cfiange the patients' position frequently. This care was 
found to be of life-saving importance, so Dr James L Wilson asi<ed for a room in which several patients could be made to breathe simulta- 
neously. A nurse could enter by the door and perform all procedures efficiently. The room pictured was built at the Children's Hospital in 
Boston, U.S.A., and was used successfully during several epidemics. Reprinted, with permission of JH Emerson Co. 



through] this copper wool which you've seen in our machines. 
First, the main reason he put the wool in was because it was 
conductive. It would conduct the heat farther up the line, closer 
to the patient, and keep the humidity high and warm. He 
couldn't get any of the big manufacturers interested in mak- 
ing this thing for him. so one day I got a call from him. He 
wanted to know if I was interested, and I said "Surely." I went 
down to see him. and he told me why he built it and said he 
thought the people would want this thing. 

So. we went back and worked on it for a year. I was involved 
in making underwater swimming stuff for the Navy, and I'd 
done that because the iron lungs had dropped out of the pic- 
ture, pretty much, because of the vaccine. So it took us about 
a year to get a machine that we thought was about right. Ben- 
son wanted equal inhalation/exhalation time. He .said he didn't 
want to worry about trying to have that variable. It was just 
a crank and a piston. Just as I was almost ready to take it down 
and show it to Benson. I get a call from Pontoppidan. Well, 
he'd been working here on a piston, I think he had Harvard 
Apparatus [a company at Harvard] get some electronic cir- 
cuits made so that he could have I-E ratio variable. We knew 
from the polio days that with some of their cases, they wished 
they could have it not equal. So. I realized it was an impor- 
tant thing. We decided we'd hold up and try to add Pontop- 
pidan's on top of what we made for Benson. That was the way 
the 3-PV came about. 

You see. all the things I've done have been because doc- 
tors have come to me with something they were trying to do. 



We didn't set out and say. "Now we're going to get in this 
field and make this." It" s because of what doctors asked me 
for. That's the way my business is run. 

Now, the next step I want to explain to you is why you're 
doing a lot of things you're doing now for rescue — the car- 
diac resuscitation you're doing as opposed to what was being 
done back then. In those days, they used Schafer prone pres- 
sure for breathing, and a few people were questioning that. 
Researchers were saying. "Well, it doesn't even move the dead 
space. How can you ventilate a patient that way?" So. at any 
rate, the Army had a problem with chemical casualties. A friend 
of mine, Jim Elam. an anesthesiologist, also. I think he was 
in Chicago, for his tour with the army, he went down to Edge- 
wood Chemical Center with a Dr Clements (you've proba- 
bly heard of Clements — he's now at the University of Cal- 
ifornia at San Francisco) to try to find out how to save these 
chemical casualties, and the way they started, he asked if I'd 
let them have a resuscitator. 

Now. our resuscitator was pressure-limited. Went up to 
1 8-cm positive pressure, and it went down to a negative phase 
of 9 cm. and went back and forth. Six months later he called 
me up and said. "We aren't getting anywhere. Those dogs all 
die. We give them the gas and we can't resuscitate them. I 
wonder whether you could make that thing go to any higher 
pressures." I said. "Sure." He said. "Well, make one that goes 
to 50 for me." And the dogs all lived! This was supposed to 
be a pressure that was dangerous. Of course everyone under- 
stands it now, but they didn't then. That if the patient's stiff 



Respiratory Care • July 1998 Vol 43 No 7 



579 



Some Reflections on Iron Lungs and Other Inventions 



enough, it's perfectly safe to put the high pressure on. 

So a big meeting was called down there, and for one thing 
they decided that they ought to throw out the Schiifer prone 
pressure, and Elam and Clements were advocating mouth- 
to-mouth, because that's about all you'd have out on the bat- 
tlefield, and you could generate enough pressure to save these 
cases, they felt. So. the meeting. I think NIH [National Insti- 
tutes of Health] held it in Washington, and Dr Whittenberger 
was chainnan. Now. Whittenberger was at the School of Pub- 
lic Health here. He u.sed to visit our place up in Essex with 
his family. One day. just before the meeting, he said to me. 
"You know, a dog when he pants, he doesn't move more than 
a seventh (I think he said a seventh) of his dead air space. But 
the dog lives. Maybe it isn't as serious as they're trying to say 
about the Schiifer." 

That triggered something with me. It got me thinking about 
high frequency, about rapidly vibrating. I got so excited about 
that that 1 got a patent back then. I guess you know I got a 
patent around 1955. 1 made a machine to do this, but I couldn't 
really get anyone too much interested in it. But that was the 
reason, and people ask me why I did this, you see. 

The other thing that was going on down there in Baltimore, 
of course, you know about Kouwenhoven, an electrical engi- 
neer at Hopkins. He was having trouble with the doctors, too. 
I mean. I don't know why I say 'too.' but ... he would go to 
meetings, showing how he could push on the sternum of a dog 
and circulate blood. Up to that time, the doctors had been — 
if you had to try to start the heart up — they'd been chopping 
you open and grabbing your heart and squeezing it. Now. these 
two things were put together, and that's what makes your pre- 
sent cardiopulmonary resuscitation. 

The next addition to our machine, we went down to 
Gainesville in Florida, and Dr Downs and Dr Kirby ... I'm 
going to back up a little bit. because I believe that before that, 
again in this hospital, they were trying to get heat, and we made 
some things for them to retard inhalation, but the people in 
Gainesville were using what they called 'constant positive pres- 
sure.' Now. I go to my father's thing, which Barach said to 
him was the classic paper on CPAP (continuous postive air- 
way pressure]. Alvin Barach had been trying to get people 
to see the value of positive pressure, constant positive pres- 
sure. In 1940. well, he wrote a lot about it. but I think my 
father's paper.* well, it was the earliest thing he could find 
where the suggestion of raising the pressure somewhat could 
be beneficial. 

Anyway. Downs and Kirby had our ventilators down there, 
but they wanted, they were trying to get manufacturers to put 
constant positive pressure, be able to raise the pressure. CPAP 
they called it. Puritan Bennett wasn't interested. They said. 



* Emerson HA. Artificial respiration in the treatment of edema ot tlu- 
lungs: a suggestion based on animal experimentation. Arch Intern 
Med I909;3:.'?68-37I. Reprinted on Pages .S8.^-.S84 in this issue, with 
permission. 



"We're selling our machines. We don't care about it ... " For- 
rest Bird was working on it for Downs and Kirby. and so, of 
course, he had it. He made the one for Kirby for babies, but 
was unable to come up at that time with one for adults. And 
so, that's when they came and said "Can't you make this 
machine to be positive?" So, the next step was adding that 
to our machine. Of course, our machine was far better suited 
for it than any other machines there were on the market, because 
they all had pumps that they can shove gas through so they're 
small piping systems, and our machine was already made so 
you could breathe very, very freely, and I think that's one of 
the great benefits — I guess you all know that — of our sim- 
ple machine that we have, ventilator. So we added that on to 
the machine, and now I don't know what else there is on it. 
Kirk, you tell me. 

Kirk: Well, there's updated alarm systems. 

Emerson: Oh, alarms, 1 haven't talked about. I had the first 
patent on the alarni for a ventilator. I believe, on the iron lung, 
and I had a lot of misgivings about it. and I still have a lot of 
misgivings. To tell the truth. I think you've got your venti- 
lators so complex that there's a lot of trouble ahead. Do many 
of you people know about the present ... problems [of a ven- 
tilator manufacturer]? You do? Well, they are the little pis- 
ton machines. They've jammed [the components] in .so small 
and tried to add so much into them, that they can't keep them 
running. Now. the big machines, of course. I think we still 
have the most reliable breathing machine or ventilator on the 
market. We had troubles, but they've got so much electronic 
stuff that it's prone to breaking down, and then they try to make 
up for it by putting a whole bunch of alarms on, and before 
you get through, it's a bunch of alarms and machines that just 
isn't reliable. I don't know how far you go. I've been on the 
standards committees and they're going to demand more and 
more sophistication. I think they're going to go on getting into 
more and more trouble. For instance, [for] home care, what 
[their ventilator] is for, they say ours is definitely the most 
reliable by far, our big machine, but they can't drag that into 
a home. It's too big. you see. We haven't really tried to make 
it much smaller. 

Anyway. I thought I might see if anyone had any questions, 
anything anybody would like to ask me about the history that 
I might know about. 

Unidentified Member of the Audience: We took your 
machine into a home in Somerville to help a child, who — when 
this child would go to sleep at night — would stop breathing. 
Tliis child's had this machine in the home for the past 13 years, 
and I remember going out there 1.^ years ago, to this old rick- 
ety house, dark night over there, and going into this home 
and the machine was there next to a wardrobe next to the bed, 
and this child was being ventilated. The mother called me 
because apparently the child was getting a little blue at night, 



580 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Some Reflections on Iron Lungs and Other Inventions 



and she thought the machine may need some adjustment. 
While I was watching the child being ventilated, lying there 
very quietly, this child was about a year of age, I saw the 
tubes from the child's tracheostomy to the machine wobbling 
in the breeze. I had no idea why. because I wasn't touching 
the tubes. I looked down and I saw the family cat there. He 
was clawing at the tubes. And I was trying to picture this sce- 
nario in the home with my intensive care unit ... in Bumam 
Six. It is really doing a remarkable job, and this child is 13 
years of age and has lived at home on this respirator and is 
a thriving child. He goes to a normal school. 

Emerson: Well, Children's in Philadelphia sent many children 
home on our machine, and also Children's in Chicago, and 
maybe you have, I don't know. This Children's has here. One 
of the real problems now with this [manufacturer's] machine, 
though, is that, for instance, Dr Goldberg at Children's in 
Chicago has all these people at home. He's pushed to get stan- 
dards on these things, because there have been so many prob- 
lems. Now the FDA has closed the door to this company — won't 
even let them sell parts. I can't understand that, becau.se I don't 
know how they'll resolve it. but here they have all these patients 
with machines that are breaking down, what do you do? Any- 
way. Anybody else got any questions on the history? 

Stoller: Well, what's on the horizon? I mean, given the fact 
that things are getting more and more complicated and prob- 
ably should get less and less complicated, how's it going to 
go? What do you think? 

Emerson: Well, I think they are going to find uses for high 
frequency. Is anything happening with that here? 

Unidentifled: Not a lot, no. 

Emerson: Not even with the pediatrics? 

Unidentified: They want to use it down in lithotripsy ... to 
minimize the movement of the patient who's being treated 
with the lithotripsy. 

Emerson: That's really sort of a problem, that is high fre- 
quency, because the FDA says you can't sell a machine that 
goes faster than 150 [breaths per minute]. And that isn't 
really high frequency, you see. And so everybody's con- 
fused. They don't know what they're talking about. High 
frequency really should be substantially higher than breath- 
ing rates, and Kirk and you people have used our standard 
ventilator at 150 right here in the hospital, and people aren't 
calling that high frequency. 

I've made two types of very simple high frequency 
machines. One of them is an interrupting affair, which they 
use at Children's successfully. And quite a few other places — 
down at Hershey Medical Center and Orlando General Hos- 



pital they've been using it. They've been doing it, in fact, the 
Critical Care show — this last one — had an exhibit on what 
they're doing down at the hospital in Orlando. 

Now, the other one is an oscillator, which is what I 
described originally, the motion down, just a diaphragm or 
a piston. They used that successfully at San Diego Children's 
... Mannio and ... Kopotic ... . Now the NIH has finally come 
around — Mary Ellen Avery, because of the success they had 
at Children's, was pushing to have a test, an NIH-run test. 
NIH has set up to run the test and they asked all the manu- 
facturers to bring machines down to Miami a year ago. and 
they were going to rush through getting this machine, 100 
machines, putting them in 10 hospitals, and finding out what 
happened if they put the machine on every other baby that 
needed to be ventilated in the first 24 hours. Well, there were 
about six manufacturers, and they chose a machine that had 
not been made yet. I think it's absolutely outrageous what 
they did. Getting a machine called the Hummingbird that [a 
company in Japan] agreed to make. They hadn't made it yet 
for babies. 

On Tuesday I'm going out to a meeting in Salt Lake. Dr 
Harris, a neonatologist at Temple, runs these meetings. They're 
going to have a discussion of this. I guess the NIH is going 
to be there and try to explain what they're doing — why they've 
done this. Again, Kopotic set up with our simple oscillator, 
it couldn't be simpler. And incidentally, right after the deci- 
sion to get this Japanese machine — the cost is going to be 
$30,000 per machine — you know, they really don't care. Any- 
way. I'm going to go out there and see what happens. I'm going 
to show my machine. You know, they want to have it there, 
and Kopotic and Mannio are probably going to describe the 
thing. But right after their decision. I got orders from three 
good California hospitals. Stanford, Sunshine — Dr Sunshine 
and Loma Linda — and the University of California at Irvine 
where Dr Whittenberger is. and Kopotic was going to show 
them how to use them. I don't know how they made out with 
them. I'll find out, probably, at this meeting. 

Unidentified: Two questions. The first one: in a very lim- 
ited sense, we could use on occasion in the operating room 
a high-frequency ventilator with which you can also give anes- 
thesia. I don't know if there are any on the market, but peo- 
ple have tried to put them together, but that's not currently 
available, as I understand it, for us to use. We have a high fre- 
quency ventilator in the O.R. — a small box. 

Emerson: Well, it isn't really high frequency. It doesn't go 
over 150. 

Unidentified: I don't think so ... it's a jet ventilator. It works 
for the short term, but we have no ability to give anesthesia. 

Emerson: In fact, they've been doing that this way, the same 
darned thing. I may come to do that. Well, if Kirk can tell us 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



581 



Some Reflections on Iron Lungs and Other Inventions 



what you want. I made one which they wanted, the same thing 
in Florida over at Clearwater, and I made it for them, and I 
got it back here. It's hard to work with somebody in Clear- 
water. It's too far away. If you want to try one of those slow 
kinds of things, now I've made — see, with FDA, you can't 
do these things anymore. 

Unidentified: That was my second question, actually. Could 
you give us, as you've gone through the history of what you've 
done — you went through it very quickly and it sounded a lot 
easier than it probably was — but in today's times versus in 
the 30s and 40s, the bureaucracy is so deep. 

Emerson: It's terrible. Look, I built my iron lung essentially 
in two weeks. I slept in it one night, and put a patient in it. 
And it worked, see! I don't think that the FDA should have 
been given the authority by Congress or whatever it is to put 
the identical rules that they have for drugs. I think there should 
be some control, but I don't think that they are equivalent, 
you see. I think the mechanical thing, you know better what 
it's going to do. but it's very difficult to do; in fact. I don't 
know, I often think of going out of business. Of course, 1 have 
the same trouble all the doctors have of lawsuits and stuff. 
Life is different. We're going to go on, till we get put out of 
business. 

Unidentified: It seems that there are a lot of things that are 
written that say that the nondemand valve ventilators are very 
good, but one thing I've noticed is that some of the other ones 
are much prettier than yours. How much is appearance impor- 
tant in your sales or in sales of ventilators? 

Emerson: Oh. I hear a lot of that. 

Unidentified: I think the Emerson is pretty. 

Emerson: I don't know what to say about that, I know the 
old green machine looked like a household appliance. But it 
worked. 

Unidentified: Do you find that the hospitals would get rid 
of those, even if they were still working, to get a new machine? 



Emerson: All right, that brings up another story. Who's going 
to ... He isn't here anymore? Who's going to Cleveland Clinic? 

Stoller: Oh, I am. 

Emerson: Oh, there you are! I was looking for you. 

Stoller: I had to sit down. 1 was going to ... 

Emerson: Who Ciime from this hospital and took over the anes- 
thesiology department at Barnes? 

Stoller: Bill Owens. 

Emerson: Bill Owens! I was trying to think of his name. Well 
it seems to me that maybe the same thing's going to happen 
at Cleveland Clinic that happened at Barnes. Bill Owens 
trained here, right? And he went down there and he threw 
all their MA- 1 "s out for his intensive care unit. He went down 
to the cellar and found about 1 8 of our machines that they 
had discarded. He brought them up, and they did a show them- 
selves. They painted them: they looked like Rolls Royces. 
They have padded covers that go over them. They're beau- 
tiful! And that's what they use in their intensive care. Now. 
I understand that in Cleveland Clinic, they had an anesthe- 
siologist who used our machine for all their anesthesia for 
their heart surgery. They simply fed anesthetic gas into it. 
And then he left. They threw them all out. It's an awfully inef- 
ficient system, I must say. Maybe you've got someone here 
who's going to ... 

Stoller: I'll give you an update. 

Emerson: So, anymore questions? 

Unidentified: Was James Wilson the same James Wilson who 
went to Michigan as chairman of pediatrics? 

Emerson: Absolutely wonderful guy! Yeali. He got me stalled 
on the iron lung. I think I've gone over time. 



582 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Ai tificial Respiration in the Treatment of Edema of the Lungs: 
A Suggestion Based on Animal Experimentation 



Haven Emerson AM MD 
New York 



On three separate occasions, in 1906, 1907 and 1908, while 
demonstrating the effects of extreme peripheral resistance on 
the heart and pulmonary circulation, 1 have noticed a definite 
result of artificial respiration when administered to an ani- 
mal apparently dying from acute pulmonary edema. 

The physical causes of the benefit apparently derived from 
this procedure seem to agree so well with facts already accepted 
in physiology, and the possibility of application of the method 
in certain kinds of clinical cases seems so reasonable, that I 
offer this communication in the hope that practical tests may, 
before long, be sufficiently conclusive to establish its value 
therapeutically, or to relegate it to the mass of theories that 
have failed. 

It will save time if I call attention to a few points regard- 
ing the effect of respiration on the circulation. The respira- 
tory fluctuations in blood pressure which anyone can appre- 
ciate in the radial pulse are due to the variation in the ease of 
passage of blood between the right and left side of the heart 
and to the inherent elasticity of the lungs. The expansion of 
the lungs allows a wider path for the blood and an increase 
in the blood in the pulmonary vessels, and at the same moment 
a diminished resistance to the passage of the blood through 
the lungs, a lessened burden for the right ventricle. When the 
lungs collapse in expiration, the elastic recoil empties the pul- 
monary vessels, and at the same time narrows the path through 
which the right ventricle must now puinp the blood. So we 
find in the last two thirds of inspiration and the first third of 
expiration a rising pressure, the remainder of the respiratory 
cycle showing a falling pressure. 

If we watch the results of positive pressure respiration prop- 
erly applied, we notice an entire reversal of the blood pres- 
sure changes above described. During the inspiratory phase, 
which is due to the forcing of air into the lungs under posi- 



From the Department of Physiology of the College of Physicians and Sur- 
geons of Columbia University in the City of New York. Read at the meet- 
ing of the Section on Medicine of the New York Academy of Medicine. 
March 16, 1909. 

Reprinted with permission of the American Medical Association from the 
Archives of Internal Medicine. Vol 3; 1909:368-371. 



live pressure, the normal conditions in the chest and in the 
pulmonary spaces are altered. The positive pressure exerted 
on the vessels in the lungs tends to empty them, or at least to 
obstruct their lumen, by just the amount of pressure exerted. 
The small vessels are squeezed, as it were, against the resis- 
tant pulmonary tissue, by air forced into the terminal vesicles 
through the trachea. During the expiratory phase the release 
from positive pressure permits a filling of the vessels again 
and a diminished resistance to the passage of blood from the 
right to the left heart. So it will be found that during positive 
pressure respiration, the so-called artificial respiration of lab- 
oratory procedure, the blood pressure falls during inspiration 
and rises during expiration. 

For our present purposes the important thing to bear in mind 
is that rhythmical variation of pressure, applied at any point 
of the circulation, will serve to assist in the onward movement 
of the blood, and will in proportion to its extent assist the action 
of the heart. It has been found possible to continue a circu- 
lation of the blood simply by artificial respiration in an ani- 
mal in which the heart is no longer capable of contracting, 
the valves allowing an onward movement with each inspi- 
ratory phase and preventing any regurgitation to fill the ves- 
sels during expiration. 

If we modify the procedure of Professor Leo Loeb, who 
first called my attention to the use of adrenalin to cause edema 
of the lungs, we can develop gradually an acute cardiac insuf- 
ficiency. Massive and repeated doses of adrenalin given intra- 
venously in a cat will produce acute dilatation of the left ven- 
tricle, due to sudden and extreme constriction of all the systemic 
arteries. The dilatation of the left ventricle allows of a mitral 
regurgitation, an acute congestion of the lungs and a dilata- 
tion and failure of the right heart. The inability of the right 
ventricle to force the blood received from the auricle against 
the back pressure of blood regurgitating from the left auri- 
cle allows of increase in the stagnation of the pulmonary cir- 
culation. Edema — that is, a collection of blood serum in the 
air spaces of the lungs — occurs, increasing until pink or clear 
serous frothy fluid appears in the trachea. Respiratory move- 
ments become exaggerated and later feeble and spasmodic, 
and the animal will presently die of asphyxia due to a flood- 



Respiratory Care • July 1998 Vol 43 No 7 



583 



ARTIFICIAL RESPIRATION IN THE TREATMENT OF EDEMA OF THE LUNGS 



ing of the air spaces of the lungs by blood serum. 

If. when we find respiration showing definite signs of begin- 
ning asphyxia, when the veins are becoming distended and 
deepened in color, cardiac insufficiency is established and the 
incompetency is increasing, and when we can hear moist rales 
over the lungs, and when we know that cardiac insufficiency 
is established and the incompetency is increasing, we then apply 
artificial respiration through the tracheotomy tube, gently dis- 
tending the lungs and allowing them to collapse with or with- 
out suction, we shall find presently an amelioration in the ani- 
mal's condition. The full expansion of the lungs, due to 
distention from within, forces a considerable amount of blood 
onward to the left auricle, and as the respiratory phase extends 
over two or three heart beats, an increased amount of blood 
will have passed the mitral valve and there will be more room 
in the pulmonary vessels when expiration occurs for the blood 
held in the distended right ventricle, and a diminished resis- 
tance in the lungs against which the right ventricle can now 
successfully empty itself. 

This at least seems the probable explanation for the improve- 
ment in the circulation which presently occurs. The lungs appear 
free from moist rales, the heart beats more vigorously, the dis- 
tention of right and left side diminishes and when the artifi- 
cial respiration is discontinued after about half an hour the 
animal is able to breathe nomially and shows none of the signs 
of insufficient circulation or respiration. The effect of the 
adrenalin has worn off, the heart muscle has recovered from 
its acute overloading, the pulmonary circuit is no longer 
engorged with regurgitated blood, and to all intents and pur- 
poses the heart and lungs aie again performing their functions 
normally. 

The bearing of this purely experimental procedure on the 
individual case of edema of the lungs in the human subject 
may not appear quite clear, and I shall try to point out the 
conditions in which 1 believe this lesson can be applied with 
advantage. 

In many instances a hypertrophied and properly com- 
pensating heart, which has adjusted itself gradually to a valvu- 
lar defect or to an increasing inelasticity of the arteries or per- 



sistent increase of peripheral resistance from any one of a num- 
ber of causes, will, if a sudden strain is put on it, develop an 
acute incompetence. Overexertion physically, overindulgence 
in food or wine, excess of psychical excitement or an unfor- 
tunate combination of all three, or an attack of contracted arter- 
ies or bronchi may be the detemiining factor. With a heart just 
able to maintain its competence under favorable conditions, 
even if it is not the seat of myocardial degeneration, insuf- 
ficiency is easily precipitated and pulmonary edema is likely 
to be developed unless the failing heart action is of very brief 
duration. Under such conditions as I have above described, 
1 believe it would be a valuable aid to the necessary medication 
if artificial respiratory movements were used. With the patient 
in the semirecumbent position, which is usually assumed when 
cardiac dyspnea is marked, raising the arms above the head 
and then pressing them against the sides of the thorax or. bet- 
ter, across the upper part of the abdomen, ought to establish 
the accessoi-y pumping action which, under nonnal conditions, 
facilitates the flow of blood through the lungs, but which the 
patient, in his enfeebled condition, is unable to do for him- 
.self. This assistance, I believe, should prove more prompt and 
effective than any medication, and would at least be giving 
mechanical relief to the overloaded heart muscle, while arte- 
rial relaxation and cardiac stimulation are being accomplished 
by drugs. 1 think such treatment would be indicated when- 
ever the edema and cardiac incompetence are of sudden devel- 
opment and ai-e due to causes which are likely to prove of brief 
duration or can be removed by appropriate treatment. Edema, 
when due to cardiac failure in the course of pneumonia or 
appearing as the inevitable tenninal feature of a chronic endo- 
carditis, could not be expected to respond to such temporary 
relief as artificial respiration would offer. Moreover. I hope 
1 shall not be misunderstood as advocating forced respiration 
by intubation or tracheotomy, for I certainly think such mea- 
sures would be quite unjustifiable. My belief, based on exper- 
imental observations, is that artificial respiratoiy movements, 
directed to establishing a rhythmical expansion and contraction 
of the thorax, are worthy of clinical trial in cases of acute car- 
diac insufficiency accompanied by edema of the lungs. 



584 



RESPIRATORY CARE • JULY 1998 VOL 4.^ NO 7 



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RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



585 



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a AARC97 52 Mechanical Ventilation: The Next 50 Years, 
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A NightinKale's Song: Outcomes of Pediatric 
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Liquid Ncntilation: From the Abyss to the Bedside, 
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Medicare Denials: The Payer's Perspective, 
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Medicare Denials: The Provider's Perspective, 
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Reimbursement of Respiratory Care Services in 
Skilled Nursing Facilities, Gary A. Graver 
Fraud and Abuse Activities in Post-acute Care 
Settings and Their Effect on Respiratory Care; 
Panel Discussion, Panelists: K. C<nnish. T. Carter G. 
Graver, M. Welch 

Five Things I Learned This Year about Lung- Volume- 
Reduction Surgery/Five Things I Learned This Year 
About Creating Credibility Outside Respiratory 
Care, Catherine M. Foss/Baihara L. Butler 
Five Things I Learned This Year about the Ti^atment 
of COPD/Five Things I Learned This Year About 
Point-of-Care Testing, DavidJ. Piersoii/Catheiine M. Foss 
Five Things I Learned This Year about Patient 
Compliance through Education, Gretchen Lawrence 
Your Profession: Agency Updates - AARC- 
JRCRTE-NBRC, Kern,- E. George. Carole J. Miller 
Benjamin F. George 

Part 1-Ventilator-Associated Pneumonia: 
Pathogenesis and Risk Factors, Marin H. Kollef 
Part 2-The Prevention of VAP in the Year 2000, 
Marin H. Kollef 

The Bronchial Provocation Challenge: Meeting the 
ATS Guidelines, Charles G. Ir\in 



□ AARC97-92 Successful Strategies for Blood Gas Labs to Meet 

the Regulations (JCAHO, CAP, CLIA) and Pass 
Inspections, Sharon S. Ehrmever 

□ AARC97 93 Pulmonary Function Testing: What Do You Need 

and When Do You Need It'.', Charles G. Inin 
Q AARC97-94 How Can I Manage the Information Explosion?, 

Shellex C. Mislioe 
LI AARC97 95 How Can I Tell If What They Say Is True?, 

Joseph L. Pail 
a AARC97-96 What Do The Numbers Mean?, Cry'stal L. Dunlevy 

□ AARC97-97 Part 4-Exercise: Normal and Abnormal Responses 

and How To Use Them, Robert B. Schoene 

□ AARC97-99 Report from the 1996 Consensus Conference, 

Neil R. Maclntyre 

□ AARC97-1(X) What Do I Need To Know about the Lung 

Transplant Patient?, Patricia Ann Doorley 
Q AARC97-10I Ventilator Care Should Be Done by Credentialed 
and 102 Respiratory Practitioners/Point-of-Care Testing 

Improves Outcomes, Kaien J. Stewart. Robert M. 

Kacinarek. Sharon S. Ehrmeyer Susan B. Blonshine 
a AARC97-103 The 6-Minute Walk Is Nothing When Compared to a 
and 104 Complete Exercise Evaluation/Charting Should Be 

Done by Exception Instead of by Conventional 

Means, Carl Mottram, Gretchen Lawrence. Patricia 

Ann Doorley. Gary W. Kauffinan 

□ AARC97-105 Managed Care Curricula, Shelley C Mishoe 

□ AARC97-106 Wellness and Disease-Prevention Curricula, 

William F. Galvin 
Q AARC97-107 Disease Management Curricula, Joseph L. Rau 

□ AARC97-108 Gerontology Curricula, Helen M. Sorenson 

a AARC97-I09 Smoking Cessation Curricula, Cnstal L Dunlevy 
Q AARC97-I10 Guidelines for the Diagnosis and Management of Asthma: 
The P'xpert Panel Report II, .Allan T. Luskin 

□ AARC97-111 Impact on Quality of Life: Recent Advances in 

Asthma Management, Andrew P. Greening 

□ AARC97-112 Safety and Efficacy of Steroids in Asthma, 

Allan T. Luskin 

□ AARC97-113A A Cost-Effective Program for Children 

Hospitalized with Asthma, Timothy R. Myers 

□ AARC97-113B Panel Discussion: Drugs and Medications - What's 

Right and What's Wrong, Andrew P. Greening. 
.Allan T. Luskin. Timothy R. Myers 

□ AARC97- 1 1 4 Pre-hospital and Inter-hospital Ti-ansport, Jeriy .4. Focht 
Q AARC97- 1 1 5 Ventilation during Transport and Diagnostic 

Studies in Acute Care Hospital, Robert S. Campbell 

□ AARC97- 116 Ventilatory Support in the Operating Room, 

Charles G. Diirbin. Jr 

□ AARC97- 1 1 7 Use of Ventilators in the Home, Robert M. Kacinarek 



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Clinical Practice Guidelines 



CPG 1 — Spirometry, 1996 Update ■ $1 

CPG 2 — Oxygen Therapy in Acute Care Hospital • $1 

CPG 3— Nasotracheal Suctioning • $1 

CPG 4 — Patient-Ventilator System Checks • $1 

CPG 5 — Directed Cough • $1 

CPG 6 — In-Vitro pH and Blood Gas Analysis and 

Hemoximetry ■ $1 
CPG 7 — Use of Positive Airway Pressure Adjuncts to 

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CPG 9 — Endotracheal Suctioning of Mechanically 

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CPGll — Postural Drainage Therapy • $1 
CPG12 — Bronchial Provocation • $1 
CPG13 — Selection of Aerosol Delivery Device ■ $1 
CPG14 — Pulse Oximetry ■ $1 
CPG15 — Single-Breath Carbon Monoxide Diffusing 

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CPG 16 — Oxygen Therapy in the Home or Extended Care 

Facility • $1 
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CPG2G — Neonatal Time-Triggered, Pressure-Limited, 

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CPG27 — Static Lung Volumes • $1 
CPG28 — Surfactant Replacement Therapy • $1 
CPG29 — Ventilator Circuit Changes ■ $1 
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Calorimetry during Mechanical Ventilation ■ $1 
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CPG32 — Body Plethysmography ■ $1 
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CPG43 — Selection of an Oxygen Delivery Device for 

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MEl3JfccH 



For VOLUNTARY reporting; 

by health profc.ssit>nals oi adverse 

events and product problems 



Form Approved 0MB No 0910-0291 E 
See 0MB staten 
FDA Use Only (Resp Care) 



Ihim Al CRODUt IS RfiPDRTINC PKOt.R/l 



A. Patient information 



I. Patient identifier 



Age at time 
of event: 



Date 
of birth: 



3 Sex 

I I female 
Dmale 



Page 



4 Weight 



B. Adverse event or product problem 



1, [ ] Adverse event 



j I Product problem (e g , detects/malfunctions) 



2. Outcomes attributed to adverse event | — , 

(check all that apply) LJ disability 

rn (jeaif, n congenital anomaly 

I — I imo/dayyri [^ required Intervention to prevent 

I I life-threatening permanent impairment/damage 

I I hospitalization - Initial or prolonged Q other: 



3 Date of 
event 



4 Date of 
this report 



5 Describe event or problen 



Relevant tests/laboratory data, including dates 



7. Other relevant history, including preexisting medical conditions (e g , allergies 
race, pregnancy, smoking and alcohol use. hepaiic/renal dysfunction, etc ) 



r 

DA Form 3500 1/96) 



Mall to: MHDWaTCH or FAX to: 

5600 Fishers Lane 1 -800-FDA-01 78 

Rockville, MD 20852-9787 



C. Suspect medication(s) 



1 Name (give labeled strength & mfr/labeler, it known) 



2 Dose, frequency & route used 



3 Therapy dates (if unknown, give duration) 



4 Diagnosis for use (indication) 



6 Lot # (if known) 



7 Exp. date (if known) 



9 NDC # (for product problems only) 



5 Event abated after use 
stopped or dose reduced 



#2 Dyes n no Dgggpy"'' 



8 Event reappeared after 
reintroduction 

#1 Dyes n™ n&'' 



#2 Dyes n™ Digify"'' 



10 Concomitant medical products and therapy dates (exclude treatment of event) 



D. Suspect medical device 



1 Brand name 



2 Type of device 



3 Manufacturer name & address 



model # _ 
catalog # 

serial # 

lot# 



other # 



4 Operator of device 

I I health professional 
I I lay user/patient 
I I other: 



5 Expiration date 



7 If implanted, give date 

(mo/day/yr) 



8, If explanted. give date 



9 Device available for evaluation? (Do not send to FDA) 
I I yes LH ho \_\ returned to manufacturer on 



1 Concomitant medical products and therapy dates (exclude treatment of event) 



E. Reporter (see confidentiality section on back) 



1 Name & address 



2 Health professional? 

□ yes □ no 



3 Occupation 



5 If you do NOT want your identity disclosed to 
the manufacturer, place an " X " in this box. QJ 



4 Also reported to 

I I manufacturer 
I I user facility 
I I distnbutor 



Submission of a report does not constitute an admission that medical personnel or the product caused or contributed to the event. 



ADVICE ABOUT VOLUNTARY REPORTING 



Report experiences with: 

• medications (drugs or biologies) 

• medical devices (including in-vitro diagnostics) 

• special nutritional products (dietary 
supplements, medical foods, infant formulas) 

• otfier products regulated by FDA 

Report SERIOUS adverse events. An event 
is serious wlien the patient outcome is: 

• deatfi 

• life-threatening (real risk of dying) 

• hospitalization (initial or prolonged) 

• disability (significant, persistent or permanent) 

• congenital anomaly 

• required intervention to prevent permanent 
impairment or damage 

Report even if: 

• you're not certain the product caused the 
event 

• you don't have all the details 

Report product problems - quality, performance 
or safety concerns such as: 

• suspected contamination 

• questionable stability 

• defective components 

• poor packaging or labeling 

• therapeutic failures 



How to report: 

• just fill in the sections that apply to your report 

• use section C for all products except 
medical devices 

• attach additional blank pages if needed 

• use a separate form for each patient 

• report either to FDA or the manufacturer 
(or both) 

Important numbers: 

• 1-800-FDA-0178 to FAX report 

• 1-800-FDA-7737 to report by modem 

• 1-800-FDA-1088 to report by phone or for 

more information 

• 1 -800-822-7967 for a VAERS form 

for vaccines 

If your report involves a serious adverse event 
with a device and it occurred in a facility outside a doc- 
tor's office, that facility may be legally required to report to 
FDA and/or the manufacturer. Please notify the person in 
that facility who would handle such reporting. 

Confidentiality: The patient's identity is held in strict 
confidence by FDA and protected to the fullest extent of 
the law. The reporter's identity. Including the identity of a 
self-reporter, may be shared with the manufacturer unless 
requested otherwise. However, FDA will not disclose the 
reporter's identity in response to a request from the 
public, pursuant to the Freedom of Information Act. 



The public reporting burden for this collection of information 
has been estimated to average 30 minutes per response, 
including the time for reviewing instructions, searching exist- 
ing data sources, gathering and maintaining the data needed, 
and completing and reviev^/ing the collection of information- 
Send comments regarding this burden estimate or any other 
aspect of this collection of information, including suggestions 
for reducing this burden to: 



DHHS Reports Clear; 



ngton, DC 20201 



Please do NOT 
return this form 
to either of these 
addresses. 



J,S DEPARTfWENT OF HEALTH AND HUMAN SERVICES 



FDA Form 3500-back 



Please Use Address Provided Below - Just Fold In Thirds, Tape and Mail 



Department of 

Health and Human Services 

Public Health Service 

Food and Drug Administration 

Rockville. IVID 20857 

Official Business 

Penalty for Private Use S300 



NO POSTAGE 

NECESSARY 

IF MAILED 

IN THE 

UNITED STATE 

OR APO FPO 



BUSINESS REPLY MAIL 

FIRST CLASS MAIL PERMIT NO. 946 ROCKVILLE, MD 



POSTAGE WILL BE PAID BY FOOD AND DRUG ADMINISTRATION 



MElJ^TCH 



The FDA Medical Products Reporting Program 
Food and Drug Administration 
5600 Fishers Lane 
Rockville, MD 20852-9787 



l,,l,lll,Hlnl,ililii.l.ll>lMlM,ll..l.l...lnl.ll 



RE/PIRATORy CORE 



Manuscript Preparation Guide 



General Information 

Respiratory Care welcomes original manuscripts related to the 
science and technology of respiratory care and prepared accord- 
ing to these Instructions and the Uniform Requirements for 
Manuscripts Submitted lo Biomedical Journals [Respir Care 1997; 
42(6):623-634]. Manuscripts are blinded and reviewed by pro- 
fessionals who are experts in their fields. Authors are responsible 
for all aspects of the manuscript and receive galleys to proofread 
before publication. Each accepted manuscript is copyedited so that 
its message is clear and it conforms to the Joumal's style. F*ublished 
papers are copyrighted by Daedalus Inc and may not be published 
elsewhere without permission. 

Editorial consultation is available at any stage of planning or writ- 
ing. On request, specific guidance is provided for all publication cat- 
egories. To receive these Instructions and related materials, write 
to RESPIRATORY CARE, 600 Ninth Avenue, Suite 702, Seattle WA 
98104, call (206) 223-0558, or fax (206) 223-0563. 

Publication Categories & Structure 

Research Article: A report of an original investigation (a study). 
It includes a Title Page, Abstract, Introduction, Methods, Results, 
Discussion, Conclusions, Product Sources, Acknowledgments, Ref- 
erences, Tables, Appendices. Figures, and Figure Captions. 

Evaluation of Device/Method/Technique: A description and eval- 
uation of an old or new device, method, technique, or modification. 
It has a Title Page, Abstract. Introduction, Description of De- 
vice/Method/Technique, Evaluation Methods, Evaluation Results, 
Discussion, Conclusions, Product Sources, Acknowledgments, Ref- 
erences, Tables, Appendices, Figures, and Figure Captions. Com- 
parative cost data should be included wherever possible. 

Case Report: A report of a clinical case that is uncommon, or was 
managed in a new way. or is exceptionally instructive. All authors 
must be associated with the case. A case-managing physician must 
either be an author or furnish a letter approving the manuscript. Its 
components are Title Page. Abstract. Introduction. Case Summa- 
ry. Discussion. References. Tables. Figures, and Figure Captions. 

Review Article: A comprehensive, critical review of the literature 
and state-of-the-art summary of a pertinent topic that has been the 
subject of at least 40 published research articles. Title Page. Out- 
line. Introduction. Review of the Literature. Summary. Acknowl- 
edgments. References. Tables. Appendices, and Figures and Cap- 
tions may be included. 

Overview: A critical review of a pertinent topic that has fewer than 
40 published research articles. 

Update: A report of subsequent developments in a topic that has 
been critically reviewed in this Journal or elsewhere. 



Point-of-View Paper: A paper expressing personal but substanti- 
ated opinions on a pertinent topic. Title Page. Text, References. Tables, 
and Illustrations may be included. 

Special Article: A pertinent paper not fitting one of the foregoing 
categories may be acceptable as a Special Article. Consult with the 
Editor before writing or submitting such a paper. 

Editorial: A paper drawing attention to a pertinent concern; it may 
present an opposing opinion, clarify a position, or bring a problem 
into focus. 

Letter: A signed communication, marked "For publication," 
about prior publications in this Journal or about other pertinent top- 
ics. Tables and illustrations may be included. 

Blood Gas Comer: A brief, instructive case report involving blood 
gas values — with Questions. Answers, and Discussion. 

Drug Capsule: A mini-review paper about a drug or class of drugs 
that includes discussions of pharmacology, pharmacokinetics, 
and pharmacotherapy. 

Graphics Corner: A briefcase report incorporating waveforms for 
monitoring or diagnosis — with Questions, Answers, and Discussion. 

Kittredge's Comer: A brief description of the operation of respiratory 
care equipment — with information from manufacturers and edito- 
rial comments and suggestions. 

PFT Corner: Like Blood Gas Comer, but involving pulmonary 
function tests. 

Cardiorespiratory Interactions. A case report demonstrating the 
interaction between the cardiovascular and respiratory systems. It 
should be a patient-care scenario; however, the case — the central 
theme — is the systems interaction. CRI is characterized by figures, 
equations, and a glossary. See the March 1996 Issue of RESPIRA- 
TORY Care for more detail. 

Test Your Radiologic Skill: Like Blood Gas Comer, but involv- 
ing pulmonary medicine radiography and including one or more radio- 
graphs; may involve imaging techniques other than conventional 
chest radiography. 

Review of Book, Film, Tape, or Software: A balanced, critical 
review of a recent release. 

Preparing the Manuscript 

Print on one side of white bond paper. 8.5 in. x 1 1 in. (216 x 279 mm) 
with margins of at least 1 in. (25 mm) on all sides of the page. Use 
double-spacing throughout the entire manuscript. Use a standard 
font (eg. Times. Helvetica, or Courier) at least 10 points in size, and 



RESPIRATORY CARE Manuscript Preparation Guide, Revised 2/98 



Manuscript Preparation Guide 



do not use italics except for special emphasis. Number all pages in 
upper-nght comers. Indent paragraphs 3 spaces. Do not justify. Do 
not put authors' names, institutional afTiliations or allusions to 
institutional affiliations in the text, or other identification any- 
where except on the title page. Repeal title only (no authors) on 
the abstract page. Begin each of the following on a new page: Title 
Page. Abstract. Text, Product Sources List. Acknowledgments. Ref- 
erences, each Table, and each Appendix. Use standard English in 
the first person and active voice. 

Center main section headings on the page and type them in cap- 
ital and small letters (eg. Introduction. Methods. Results. Discus- 
sion). Begin subheadings at the left margin and type them in cap- 
ital and small letters (eg. Patients. Equipment. Statistical Analysis). 

References. Cite only published works as references. Manuscripts 
accepted but not yet published may be cited as references: desig- 
nate the accepting journal, followed by (in press), and provide 3 copies 
of the in-press article for reviewer inspection. Cite references in the 
text with superscript numerals. Assign numbers in the order that ref- 
erences are first cited. On the reference page, list the cited works 
in numerical order. Follow the Journal's style for references. Abbre- 
viate journal names as in Inde.x Medicus. List all authors. 

Article in a journal carrying pagination throughout volume: 

Rau JL. Harwood RJ. Comparison of nebulizer delivery methods 
through a neonatal endotracheal tube: a bench study. Respir Care 
1992:37(11): 1233- 1240. 

Article in a publication that numbers each issue beginning with 
Page 1 : 

Bunch D. Eistablishing a national database for home care. AARC Times 
1991;15(Mar):61,62.64. 

Corporate author journal article: 

American Association for Respiratory Care. Criteria for establish- 
ing units for chronic ventilator-dependent patients in hospitals. Respir 
Care 1988:33(11): 1 044- 1046. 

Article in journal supplement: (Journals differ in their methods of 
numbering and idenufying supplements. Supply sufficient information 
to promote retrieval.) 

Reynolds HY. Idiopathic interstitial pulmonary fibrosis. Chest 1986: 

89(3Suppl):139S-l43S. 

Abstract in journal: (Abstracts citations are to be avoided. Those more 

than 3 years old should not be cited.) 

Stevens DP. Scavenging ribavirin from an oxygen hood to reduce envi- 
ronmental exposure (abstract). RespirCare 1990:3.'i( 1 1 ): 1087-1088. 

Editorial in journal: 

Enright P. Can we relax during spirometry? (editorial). Am Rev Respir 
Dis I993:148(2):274. 

Editorial with no author given: 

Negative-pressure ventilation for chronic obsUiictive pulmonary dis- 
ease (editorial). Lancet 1992;.34()(8833):1440-1441. 

Letter in journal: 

Aclony Y. Ethnic norms for pulmonary function tests (letter). Chesi 
1991:99(4): 10.51. 



Paper accepted but not yet published: 

Hess D. New therapies for asthma. Respir Care (year, in press). 

Personal author book: (For any book, specific pages should be cited 
whenever possible.) 

DeRemee RA. Clinical profiles of diffuse interstitial pulmonary dis- 
ease. New York: Futura: 1990. p. 76-85. 

Corporate author book: 

American Medical Association Department of Drugs. AMA drug eval- 
uations. 3rd ed. Litdeton CO: Publishing Sciences Group: 1977. 

Chapter in book with editor(s): 

Pierce AK. Acute respiratory failure. In: GuenterCA. Welch MH, edi- 
tors. Pulmonary medicine. Philadelphia: JB Lippincott; 1977:26-42. 

Tables. Use consecufively numbered tables to display information. 
Start each table on a separate page. Number and title the table and 
give each column a brief heading. Place explanations in footnotes, 
including all nonstandard abbreviations and symbols. Key the foot- 
notes with conventional designations (*, t, t- §. H- 1. **. tt) in con- 
sistent order, placing them superscript in the table body. Do not use 
horizontal or vertical rules or borders. Do not submit tables as pho- 
tographs, reduced in size, or on oversize paper. Use the same type- 
face as in the text. 

Illustrations. Graphs, line drawings, photographs, and radiographs 
are figures. Use only illustrations that clarify and augment the text. 
Number them consecutively as Fig. 1, Fig. 2, and so forth accord- 
ing to the order by which they are mentioned in the text. Be sure 
all figures are cited. If any figure was previously published, include 
copyright holder's written permission to reproduce. Figures for 
publication must be of professional quality. Data for the original 
graphs should be available to the Eiditor upon request. If color is essen- 
tial, consult the Editor for more information. In reports of animal 
experiments, use schematic drawings, not photographs. A letter of 
consent must accompany any photograph of a person. Do not place 
titles and detailed explanations on figures; put this information in 
figure captions. If possible, submit radiographs as prints and full- 
size copies of film. 

Drugs. Identify precisely all drugs and chemicals used, giving gener- 
ic names, doses, and routes of administration. If desired, brand names 
may be given in parentheses after generic names. Drugs should be 
listed on the product-.sources page. 

Commercial Products. In parentheses in the text, identify any com- 
mercial product (including model number if applicable) the first time 
it is mentioned, giving the manufacturer's name. city, and state or 
country. If four or more products are mentioned, do not list any man- 
ufacturers in the text; instead, list them on a Product Sources page 
at the end of the text, before the References. Provide model num- 
bers when available and manufacturer's suggested price, if the study 
has cost implications. 

Ethics. When reporting experiments on human subjects, indicate 
that procedures were conducted in accordance with the ethical stan- 
dards of the World Medical Association Declaration of Helsinki 
[RespirCare 1997;42(6):635-636] or of the institution's committee 



RESPIRATORY CARE Manuscript Preparation Guide. Revised 2/98 



Manuscript Preparation Guide 



on human experimentation. State that informed consent was 
obtained. Do not use patient's names, initials, or hospital numbers 
in text or illustrations. When reporting experiments on animals, indi- 
cate that the institution's policy, a national guideline, or a law on 
the care and use of laboratory animals was followed. 

Statistics. Identify the statistical tests used in analyzing the data, 
and give the prospectively determined level of significance in the 
Methods section. Report actual p values in Results. Cite only text- 
book and published article references to support choices of tests. Iden- 
tify any general-use or commercial computer programs used, nam- 
ing manufacturers and their locations. These should be listed on the 
product-sources page. 

Units of Measurement. Express measurements of length, height, 
weight, and volume in metric units appropriately abbreviated; tem- 
peratures in degrees Celsius; and blood pressures in millimeters of 
mercury (mm Hg). Report hematologic and clinical-chemistry mea- 
surements in conventional metric and in SI (Systeme Internationale) 
units. Show gas pressures (including blood gas tensions) in torr. 
List SI equivalent values, when possible, in brackets following non- 
Si values— for example, -PEEP, IOcmH:0[0.981 kPa]." For con- 
version to SI, see RESPIRATORY CARE 1988;33(10):86l-873 (Oct 
1988). l989;34(2):l45(Feb 1989), and 1997;42(6):639-640(June 
1997). 

Conflict of Interest Authors are a.sked to disclose any liaison or finan- 
cial arrangement they have with a manufacturer or distributor whose 
product is part of the submitted manuscript or with the manufacturer 
or distributor of a competing product. (Such arrangements do not 
disqualify a paper from consideration and are not disclosed to review- 
ers. ) A statement to this effect is included on the cover-letter page. 
(Reviewers are screened for possible conflict of interest.) 

Abbreviations and Symbols. Use standard abbreviations and sym- 
bols. Avoid creating new abbreviations. Avoid all abbreviations 
in the title and unusual abbreviations in the abstract. Use an abbre- 
viation only if the term occurs several times in the paper. Write out 
the full term the first time it appears, followed by the abbreviation 
in parentheses. Thereafter, einploy the abbreviation alone. Never 
use an abbreviation without defining it. Standard units of mea- 
surement can be abbreviated without explanation (eg, 10 L/min, 
15 torr, 2.3 kPa). 

Please use the following forms: cm HiO (not cmH20), f (not bpm), 
L (not 1), L/min (not LPM, l/min, or 1pm), mL (not ml), mm Hg (not 
mniHg), pH (not Ph or PH), p > 0.001 (not p>0.001 ), s (not sec), 
SpO: (pulse-oximetry saturation). See RESPIRATORY CARE; 
Standard Abbreviations and Symbols [RespirCare I997;42(6):637- 
642]. 

Submitting the Manuscript 

Mail three copies [I copy with author(s) name(s), affiliation(s), 2 
copies without name(s) and aftlhation(s) for reviewers] of the manu- 
script, figures, and 1 diskette, and the Cover Letter & Checklist to 
RESPIRATORY CARE, 600 Ninth Avenue, Suite 702. Seattle WA 
98 104. Do not fax manuscripts. Protect figures with cardboard. Keep 
a copy of the manuscript and figures. Receipt of your manuscript 



will be acknowledged. 

Computer Diskettes. Authors are encouraged to submit electron- 
ic versions of manuscripts as well as printed copies (3.5 in. diskettes 
in Macintosh or IBM-DOS format). Label each diskette with date; 
author's name; name and version of word-processing program used; 
and filename(s). Software used to produce graphics and tables should 
be similarly identified. Do not write on diskette labels except with 
felt-tipped pen. If revision of a manuscript is required as a condi- 
tion of acceptance for publication, we ask that an electronic version 
of revision be supplied to facilitate copyediting and production. 

Prior and Duplicate Publication. Work that has been published 
or accepted elsewhere should not be submitted. In special instances, 
the Editor may consider such material, provided that permission to 
publish is given by the author and original publisher. Please con- 
sult the Editor before submitfing such work. 

Authorship. AH persons listed as authors should have participat- 
ed in the reported work and in the shaping of the manuscript; all must 
have proofread the submitted inanuscript; and all should be able to 
publicly discuss and defend the paper's content. A paper with cor- 
porate authorship must specify the key persons responsible for the 
article. Authorship is not justified solely on the basis of solicitation 
of funding, collection or analysis of data, provision of advice, or sim- 
ilar services. Persons who provide such ancillary services exclusively 
may be recognized in an Acknowledgments section. 

Permissions. The manuscript must be accompanied by copies of 
permissions to reproduce previously published material (figures or 
tables); to use illustrations of, or report sensitive personal information 
about, identifiable persons; and to name persons in the Acknowl- 
edgments section. 

Reviewers. Please supply the names, credentials, affiliations, address- 
es, and phone/fax numbers of three professionals whom you con- 
sider expert on the topic of your paper. Your manuscript may be sent 
to one or more of them for blind peer review. 



Editorial Office: 

RESPIRATORY CARE 

600 Ninth Avenue, Suite 702 

Seattle W A 98104 

(206) 223-0558 (voice) 

(206) 223-0563 (fax) 

e-mail: rcjournal@aarc.org 

kreilkamp@aarc.org 



RESPIRATORY CARE Manuscript Preparation Guide, Revised 2/98 



COVER LETTER & CHECKLIST 

A copy of this completed form must accompany all manuscripts submitted for publication. 



Title of Paper: 



Publication Category: 



Corresponding Author: Phone: FAX: 

Mailing Address: 

Reprints: □Yes □ No E-mail Address: 



"We, the undersigned, have all participated in the work reported, proofread the accompanying manuscript, and approve its sub- 
mission for publication." Please print and include credentials, title, institution, academic appointments, city and state. If more 
than 4 authors, please use another copy of this form.* 

'First Author: 



Author Signature/Date. 



*Second Author: 



*Third Author: 



Author Signature/Date. 



Author Signature/Date. 



•Fourth Author: 



Author Signature/Date, 



Has this research been presented in any public forum? □ Yes □ No 
If yes, where, when and by whom? 



Has this research received any awards? □ Yes □ No 
If yes, please describe. 



Has this research received any grants or other support, financial or material? □ Yes □ No 
If yes, please describe. 



Do any of the authors of this manuscript have a financial interest in (or a commercial or consulting relationship to) any of the 
products or manufacturers mentioned in this paper or any competing products or manufacturers? □ Yes □ No 



If yes, please describe. 



I 



□ Have you enclosed a copy of the manuscript on diskette? 

□ Is double-spacing used throughout entire manuscript? 

□ Are all pages numbered in upper-right corners? 

□ Are all references, figures, and tables cited in the text? 

□ Has the accuracy of the references been checked, and are they correctly formatted? 

□ Have SI values been provided? 

□ Has all arithmetic been checked? 

□ Have generic names of drugs been provided? 

□ Have necessary written permissions been provided? 

□ Have authors' names been omitted from text and figure labels? 

□ Have copies of 'in press' references been provided? 

□ Has the manuscript been proofread by all the authors? 

□ Have the manufacturers and their locations been provided for all devices and equipment used? 

RliSI'IRATOKY CARH Manuscript Preparation Guide. Revised 2/98 



American Association for Respiratory Care 



Jd^\-JJ!yjJ 



Please read the eligibility requirements for each of the classifications in the 
right-hand column, then complete the applicable section. All information 
requested below must be provided, except where indicated as optional. 
See other side for more information and fee schedule. Please sign and date 
application on reverse side and type or print clearly. Processing of applica- 
tion takes approximately 15 days. 

n Active 
Associote 

D Foreign 

D Physician 

D Industrial 
D Special 
D Student 



Last Name _ 
First Name 



Social Security No. 
Home Address 



State 



-Zip 



Phone No. 



Primary Job Responsibility /check one only) 

n Technical Director 

n Assistant Technical Director 

n Pulmonary Function Specialist 

D Instructor/Educator 

n Supervisor 

D Staff Therapist 

D Staff Technician 

D Rehabilitation/Home Core 

n Medical Director 

□ Sales 

D Student 

n Other, specify 



Type of Business 

ZL Hospital 

□ Skilled Nursing Facility 

D DME/HME 

D Home Health Agency 

D Educational Institution 

C Manufacturer or supplier 

D Other, specify 



Date of Birth (optional) 



U.S. Citizen? 



. Sex (optional) 



Hove you ever been a member of the AARC? 



■ so, when? From 



^ 



For office use only 



FOR ACTIVE MEMBER 

An individual is eligible if he/she lives in ihe U S or its territories or v»as an Active Member 
prior to moving outside its borders or territories, ond meets ONE of the following criterio: (1 ) is 
legolly credentioled as o respiratory core professional if employed in a state that monOGtes 
such, OR |2) IS o graduote of on accredited educational program in respiratory core, OR (3) 
holds o credential issued by the NBRC An individuol who is on AARC Active Member in good 
standing on December 8, 1 994, will continue as such provided his/her membership remains in 
good standing. 



Place of Employment _ 
Address 



City_ 
State 



.Zip 



Phone No. ( ) 

Medical Director/Medical Sponsor 



FOR ASSOCIATE OR SPECIAL MEMBER 



Individuals who hold a posJIton reioted to r 
Active Member shall be Associate Member 
ciahon except to hold office, vote, or si 
classes of Associate Membership are i 
v/hose primary occupation is directly c 
Hon of respiratory core equipment or 
respiratory care-related field 



Place of Employment _ 

Address 

City 



but do not meet the requirements of 
'They hove oil the rights and benefits of the Asso- 
5 choir of o stonding committee The following sub- 
ond Industrial (individuals 
nufocture, sale, or distribu- 



railoble Foreign, Phy: 
indirectly devoted to the m 
upplies) Speciol Members 



. tho 



,rking 



State 

Phone No. 



-Zip 



FOR STUDENT MEMBER 

Individuals will be closstfied as Student Members if they meet all the requirements for Associate 
Membership and are enrolled in an educational program in respiratory care accredited by, or 
in the process of seeking accreditation from, an AARC-recognized agency. 

SPECIAL NOTICE — Student Members do not receive Continuing Respiratory Care Education 
(CRCE) transcripts Upon completion of your respiratory care education, continuing education 
credits may be pursued upon your redo 



1 to Active or Associate Membe 



School/RC Program 

Address 

City 



.Zip 



State 

Phone No. | ) 

Length of program 

C 1 year 
L' 2 years 



4 years 
Other, specify _ 



Expected Date of Graduation (REQUIRED 
INFORMATION) 

Preferred mailing address: H Home T" Businfii;<; Month 

American Association for Respiratory Care • 1 1030 Abies Lane • Dallas, TX 75229-4593 • [972] 243-2272 • Fax [972] 484-2720 



American Association for Respiratory Care 




Demographic Questions 

We request that you answer these questions in order to help us 
design services and programs to meet your needs. 



Checfc file Highest Degree Earned 

D High School 

n RC Graduate Technician 

D Associate Degree 

D Bachelor's Degree 

n Master's Degree 

n Doctorate Degree 



Number of Years in Respiratory Care 

a 0-2 years D 11-15 Years 

n 3-5 years D 1 6 years or more 

n 6-10 years 



Sob Status 


a 


Full Time 


a 


Part Time 


Credentials 


D 


RRT 


D 


CRH 


n 


Physician 


D 


CRNA 


a 


RN 


Salary 




D 


Less than $10,000 


D 


$10,001-$20,000 


D 


$20,001 -$30,000 


D $30,001 -$40,000 


D 


$40,000 or more 



n LVN/LPN 

D CPFT 

D RPFT 

D Perinatal/Pediatric 



PLEASE SIGN 

I hereby apply for membership in the American Association for Respirotory Care 
ond hove enclosed my dues If opproved for membership in the AARC, I will abide 
by its bylaws and professional code of ethics. I authorize investigation of all state- 
ments contained herein and understand that misrepresentations or omissions of 
facts called for is cause for rejection or expulsion, 

A yearly subscription to RESPIRATORY CARE journal and AARC Times magazine 
includes an allocotion of $1 1 ,50 from my dues for eoch of these publications. 

NOTE: Contributions or gifts to the AARC are not tax deductible as charitable con- 
tributions for income tax purposes- However, tfiey may be tax deductible as ordi- 
nary and necessary business expenses subject to restrictions imposed as a result of 
association lobbying activities. Tf\e AARC estimates that the nondeductible portion 
of your dues — the portion v/hich is allocable to lobbying — is 26%. 

Signaiure 

Date 



Membersltip Pees 






Payment must accompany your application to the 


AARC. Fees are 


for 12 


months. (NOTE: Renewal fees are $75.00 Active, Associate-Industrial o 


Associ- 


ate-Physicion, or Special status; $90.00 for Associate-Foreign status; and |, 


$45.00 for Student status). 




1 


D Active 


$ 87.50 




n Associate (Industrial or Physician) 


$ 87.50 




D Associate (Foreign) 


$102.50 


i 


n Special 


$ 87.50 




n Student 


$ 45.00 




TOTAL 
Specialty Sections 


$ 






Established to recognize the specialty areas of respiratory core, these 


sections 


publish a bi-monthly newsletter that focuses on issues 


of specific concern to that 1 


specialty. The sections also design the specialty programming at the 


national 


AARC meetings. 






D Adult Acute Care Section 


$15.00 




D Education Section 


$20.00 




D Perinotal-Pediotric Section 


$15.00 




D Diagnostics Section 


$15.00 




n Continuing Care- 






Rehabilitation Section 


$15.00 




D Management Section 


$20.00 




n Transport Section 


$15.00 




D Home Care Section 


$15.00 




D Subacute Core Section 


$15.00 




TOTAL 
GRAND TOTAL = Membership Pee 


$ 






plus optional sections 


$ 




D Total Amount Enclosed/Charged $ 






D Please charge my dues (see below) 


A 




To charge your dues, complete the following: A 


kAJ' 


> 


a MasterCard /j 


IeAII 




D Visa -^- 


T?" 


^ 


Card Number 


.MJm. 




Cord Expires / 






Signature 






1 



Mail application and appropriate fees to: 
Amsrlcon Association for Respiratory Care • 1 1030 Abies Lane • Dallas, TX 75229-4S93 • [972] 243-2272 • Fax [972] 484-2720 



Not-for-profit organizations are offered a free advertisement of up to eight lines to appear, on a space-available 

basis, in Calendar of Events in RESPIRAORY CARE. Ads for other meetings are priced at $5.50 per line and require 

an insertion order. Deadline is the 20th of the month two months preceding the month in which you wish the ad to run. 

.Submit copy and insertion orders to Calendar of Events, RESPIRATORY CARE, 1 1030 Abies Lane. Dallas TX 75229-4593. 



Calendar 
of Events 



AARC & AFFILIATES 

July 17-19 — Aiiwriciin Association for 

Respirulory Cure 
1998 Summer Foram at the Registry 
Resort. Naples, Florida. Sessions will 
cover education and management, plus 
additional topics including ■Technology 
and Credenlialing," and "The Lewin 
Group Report: Implications for the 
Respiratory Care Community." Following 
the Summer Forum, a Spirometry 
Workshop will be conducted at the same 
facility July 19-20; and participants can 
earn seven hours of CRCE credit. 
CRCE: Up to 20 hours of continuing 
respiratory care education (CRCE) credits. 
Contact: The AARC at (972) 243-2272. 



July 20-21 — Nevada Society 
Annual Conference and Business Meeting 
at the Atlantis Hotel Casino in Reno, 
Nevada. 

CRCE: 10 CRCE credits have been 
requested. 

Contact: John Steinmetz, 181 Brooks 
Circle, Sparks NV 89431, (702) 331-0721 

August 5-7 — TriState Respiratory Care 
Conference 

27th annual meeting — Changing Times; 

A Continuation — at the Grand Casino 

Biloxi Bayview Hotel, Biloxi, 

Mississippi. 

CRCE: 14 hours; nursing units have also 

been approved. 

Contact: Rocco Tretola, (504) 482-3530, 

e-mail eorr@ochsner.org, or visit the web 

site at http;//members. 

aol.com/akramer259/documents. 



August 14 — Live Teleconference 
"Care Plans: Developing, Implementing, 
and Measuring Outcomes," Part 6 of the 
AARC's 1998 "Professor's Rounds," 
from 12:30-2 pm Eastern Time. 
Contact: The AARC at (972) 243-2272. 

August 21 — Ohio Socien^ 
Independence, Ohio 
Critical Care Committee announces its 
annual seminar to be held at the Holiday 
Inn Rockside Road, Independence, Ohio. 
CRCE: 6 hours. 

Contact: Nancy Johnson, (330) 929-7166 
or abbyru@aol.com. 

September 11-13— AARC Patient 
Assessment Course 



Chicago, Illinois 

The course will be offered at the Clarion 

International Quality Inn at O'Hare, 

Chicago, Illinois. 

CRCE: 16 hours are available. 

Contact: Preregistration is required, call 

(972) 243-2272. 

September 16-18 — MaiylaniWistricl of 

Columbia Society 
1 8th Annual Conference by the Sea at the 
Sheraton in Ocean City, Maryland. Two 
certification programs, "Advanced 
Respiratory Skills for Skilled and 
Subacute Care" and "Patient 
Assessment," will also be offered. 
Contact: Jeanette Ledbetter at 
(202) 574-6348. 

October S—New York 

Societ^■-Solltheastern Chapter 
30th Annual Syinposium at the Marriott 
Marquis in Manhattan, New York, New 
York. Featured speaker is AARC 
Executive Director Sam Giordano, MBA. 
RRT, speaking on "The RCP: Practice in 
the 2 1 st Century." Also, the NYSSRC and 
SUNY Stony Brook will be hosting a 
clinical assessment workshop Oct. 9-10 at 
the Cornell Club in Manhattan. 
Contact: (5 16) 444-3 18 1 or 
www.nyssrc.org. 

October 9 — Southern Chapter of the 

Colorado Socien.' 
Fifth Annual Southern Colorado 
Pulmonary Medicine Symposium at the 
Holiday Inn Garden of the Gods. 
Colorado Springs, Colorado. 
Contact: Cathy Fletchall at (719) 776-5025 
or Barry Beard at (719) 776-5212. 

November 7-10 — International 

Respiratory Congress 
The American Association for 
Respiratory Care hosts its 44th annual 
International Respiratory Congress at the 
Georgia World Congress Center in 
Atlanta, Georgia. More than 7,000 people 
will experience programs appealing to all 
levels of health care providers — from 
clinicians to managers and administrators, 
to manufacturers and distributors of 
equipment and supplies. Program content 
will include neonatal, pediatric, and adult 
critical care; acute, continuing and 
rehabilitative care; diagnostics; 
management; and case and disease 



management — truly a comprehensive 
program on respiratory care. Exhibits by 
all manufacturers of cardiopulmonary 
equipment in the world will be featured. 
Contact: For program brochure and 
registration information, contact the 
AARC, 1 1030 Abies Lane. Dallas TX 
75229-4593; (972) 243-2272; fax (972) 
484-2720; e-mail: meetings@aarc.org; or 
visit the web site at www.aarc.org. 

OTHER MEETINGS 

August-December — National Subacute 

Care Association 
Seven, 2-day, regional seminars, covering 
Minimum Data Set (MDS) to classify 
patients in the Resource Utilization Group 
System (RUG). These will be held in 
Chicago, Illinois; Hartford, Connecticut; 
Philadelphia, Pennsylvania; Dallas, 
Texas; Seattle, Washington; Los Angeles, 
California; and Orlando, Florida. 
Contact: (301) 961-8680. 

December 9-11 — Diagnosis and 
Treatment of Sleep Breathing Disorders 
An international conference that will 
feature 50 speakers from all over the 
world with all sessions translated either 
into English or French, Grenoble, France. 
Abstracts for presentation are being 
sought and are due Oct. 1 . 
Contact: Congress Secretariat at 
ADTSAS, Hopital de la Croix Rousse, 
Service de Reanimation et d' Assistance 
Respiratoire, Hopital de la Croix Rousse. 
93 Grande Rue de la Croix Rousse, 69317 
Lyon Cedex 04, France. Phone 33 (0)4 76 
76 55 16, fax 33 (0)4 76 76 56 17, e-mail 
Patrick.Ievy@imag.fr. 

June 12-16, 1999 — International Society 

for Aerosols in Medicine 
1 2th International Congress at the Austria 
Center in Vienna, Austria. 
Contact: Vienna Academy of 
Postgraduate Medical Education and 
Research, Alser Strasse 4. A- 1090 
Vienna, Austria. Phone (-1-43/1 ) 405 13 
83-22, fax (-H43/1 ) 405 13 83-23, E-mail 
medacad@via.at. 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



597 



Notices 



Notices of competitions, scholarships, fellowships, examination dates, new educational programs. 

and the like will be listed here free of charge. Items for the Notices section must reach the Journal 60 days 

before the desired month of publication (January 1 for the March issue. February 1 for the April issue, etc). Include all 

pertinent information and mail notices to RESPIRATORY Care Notices Dept, 1 1030 Abies Lane. Dallas TX 75229-4593. 



^Itlarda 




\ Helpful UJeb.Sites 

American Association for Respiratory Care 

http://www.aarc.org 

— Current job listings 

— American Respiratory Care Foundation 
fellowships, grants, & awards 

— Clinical Practice Guidelines 

National Board for Respiratory Care 

http://www.nbrc.org 

RESPIRATORY CARE online 

http://www.rcjournal.com 

— 1997 Subject and Author Indexes 

— Contact the editorial staff 

The American College 
of Chest Physicians 

http://www.chestnet.org 



The National Board for Respiratory Care — 1998 Examination Dates and Fees 



Examination 

CRTT Examination 

RRT Examination 
RPFT Examination 



Examination Date 

November 14, 1998 

Application Deadline: September 1, 1998 

Decembers, 1998 

Application Deadline: August 1. 1998 

Decembers, 1998 

Application Deadline. September 1, 1998 



Examination Fee 

$100 (new applicant)* 

60 (reapplicant)* 

250 Both (new applicant) 

210 Both (reapplicant) 

180 (new applicant) 

150 (reapplicant) 



*In 1999, this examination fee will increase by $20. 



For information about other services or fees, write to the National Board for Respiratory Care, 
8310 Nieman Road. Lenexa KS 66214, or call (913) 599-4200. FAX (913) 54 l-0156,or e-mail: nbrc-info@nbrc.org 



.598 



RE.SPIRATORY CARE • JULY 1998 VOL 43 NO 7 



Notices 



WATCH FOR 



CRCE THROUGH 
THE JOURNAL 

respiratory care 
August 1998 



Coming Soon 

RespirdtoryCm 
Week 

October 4*- 10M998 



New Federal Register Notices Now Available 

The Center for Devices and Radiological Health announces the 
publication of new Facts-on-Demand FOD notices in the 
Federal Register. The new publications: FOD#774 — Medical 
Devices; Preemption of State Product Liability Claims; 
Proposed Rule; FOD#607 — Rebuilders, Reconditioners, 
Services, and "As Is" Remarketers of Medical Devices; Review 
and Revision of Compliance Policy Guides and Regulatory 
Requirements; Request for Comments and Information; 
Proposed Rule: and FOD#513 — Medical Devices; Reports of 
Corrections and Removals; Stay of Effective Date of 
Information Collection Requirements; Stay of Effective Date 
of Final Regulation. For more information about Facts-on- 
Demand call (800) 899-0381 or (301) 826-0111. The FOD sys- 
tem is also on the Internet at www.fda.gov/cdrh/fedregin.html. 



NAMES 1 998 Education, Conference 
Schedule Set 

The National Association for Medical Equipment Services 
(NAMES) announces its 1998 national conferences and 
regional education seminars. For information about 
upcoming events, call the NAMES Education & Meeting 
Department at (703) 836-6263, or visit the web site: 
www.names.org. 



Web Site Link to Fellowships, Scholarships, 
& Grants 

The American Association for Respiratory Care's web site con- 
tains important information about fellowships, scholarships, 
and research grants. International fellowships, education 
scholarships, research fellowships, and other grand programs 
are described in detail. The site also contains information 
about the $1,000,000 Research Fund, a restricted fund to 
sponsor research initiatives that document the clinical and 
economic impact of respiratory care professionals in the deliv- 
ery of health care. To apply, a "Research Plan Abstract" must 
be submitted to the AARC by October 1, 1998. To find out 
more about these programs, log on at www.aarc.org. 



year 2000 Date Problem Addressed by FDA 

On June 24, 1998, the Food and Drug Administration 
announced the availability of the document, "Guidance on 
FDA's Expectations of Medical Device Manufacturers Concern- 
ing the Year 2000 Date Problem." The document is available 
via telephone (800) 899-0381 or (301) 827-0111 or via the 
Internet at www.fda.gov/cdrh/yr2000/y2kguide.html. 



Consumer Information Catalog Available 

The United States General Services Administration provides a 
catalog of consumer information that may be helpful to health 
care providers. For a copy of the catalog, write to R Woods, 
CIC - 8A, P Box 100, Pueblo CO 81002, or call (719) 948-4000, 
or visit the Internet web site at www.pueblo.gsa.gov. 



RESPIRATORY CARE • JULY 1998 VOL 43 NO 7 



599 



Authors 

in This Issue 



Aggarwal. Ashutosh Nath 557 

Behera. Digamber 557 

Bishop, Michael J 552 

Branson, Richard D 567 

Emerson, Haven 583 

Emerson, John H 573 

Finley, Jennifer 552 

Gupta, Dheeraj 557 

Hess, Dean R 546 

Hussey, John D 552 

Jain, Sanjay 557 



Jindal. Surinder Kumar 557 

Joy, James 552 

Lakshminarayan, S 552 

Ludlam, Shari Eason 562 

Massey, Lewis 552 

Michnicki, Irene 549 

Ognibene, Frederick P 562 

Stolier, James K 549, 572 

Wood, Lauren V 562 

Zeidman, David 562 



Advertisers 
in This Issue 



To advenise in RESPIRATORY CARE, conlact Tim Goldsbury. 20 Tradewinds Circle, Tequesta FL 33469 
al (561) 745-6793, Fax (561) 745-6795, e-mail: goldsbury (gaarc.org, for rales and media kits. For recruitment/ 
classified advertising contact Beth Binkley, Marketing Assistant for RESPIRATORY CARE, at (972) 243-2272, 
Fax (972) 484-6010. Rick Owen is the Marketing Director for RESPIR.'^TORY CARE. 



DEY Laboratories 527 IMPACT Instniinentation, Inc Cover 3 

Circle Reader Ser\ ice No. 102 Call (800) 755-5560 Circle Reader Service No. 117 Call (201) 882-1212 

DHD Diemolding Healthcare Division Cover 4 Nellcor Puritan Bennett 530 

Circle Reader Service No. 109 Call (800) 847-8000 Circle Reader Service No. 108 Call (800) NELLCOR 

Drager Cover 2 PLASTIMED 536 

Circle Reader Service No. 122 Call (703) 817-0100 Circle Reader Service No. 123 Call (407) 672-081 1 

Hans Rudolph 541 Respironics Inc 522 

Circle Reader Service No. 104 Call (800) 456-6695 Circle Reader Service No. 120 Call (800) 638-8208 

Helen Ziegler & Assoc 534 University of Minnesota 537 

Circle Reader Service No. 1 15 Call (800) 387-4616 



Circle Reader Service No. 1 10 



Call (612) 626-7600 



Copyright information, respiratory Care is copyrighted by 
Daedalus Enterprises Inc. Reproduction in whole or in part without the express 
written permission of Daedalus Enterprises Inc is prohibited. Permission to 
photocopy a single article in this Journal for noncommercial purposes of 
scientific or educational advancement is granted. Permission for multiple 
photocopies and copies for commercial purposes must be requested in writ- 
ing, via e-mail (rcjoumal@aarc.org), or telephone and approved by RESPI- 
RATORY CARE. Anyone may, without permission, quote up to 500 words of 
material in this journal provided the quotation is for noncommercial use and 
RESPIRATORY CARE is credited. Longer quotation requires written ap- 
proval by the author and publisher. Single reprints are available only from the 
authors. Reprints for commercial use may be purchased from Daedalus En- 
terprises Inc. For inore information and prices call (972) 243-2272. 

DI.SCLAIMER. The opinions expressed in any article or editorial are those 
of the author and do not necessarily reflect the views of the Editors, the 
American Association for Respiratory Care (AARC), or Daedalus Enter- 
prises Inc. Neither are the Editors, the AARC, or the Publisher responsible 
for the consequences of the clinical applications or use of any methods or de- 
vices described in any article or advertisement. 

SUB.SCRIHTION RATE.S. Individual subscription rates are $75 per year 
(12 issues), $145 for 2 years, and $215 for .3 years in the US and Puerto 
Rico. Rates are $90 per year, $1 75 for 2 years, and $260 for .3 years in all other 
countries (add $94 per year for air mail ). Single copies when available cost 



$7; add $9 for air mail postage to overseas countries. Checks should be 
made payable to RESPIRATORY CARE and sent to the subscription office at 
1 1030 Abies Lane, Dallas TX 75229-4593. 

Subscription Rates for associations. An association may 

offer individual subscriptions of RESPIRATORY CARE to its members at a 
reduced rate. The rates based on membership are: $8.50 per year for 1 1 -5(X) 
members; $8 for 501-1,500 members: $7.50 for 1,501-10,000 members; 
$6.50 for more than 10,000 members. For information, contact Ray Mas- 
ferrer at (972) 243-2272. 

CHANGE OF ADDRESS. Notify the AARC at (972) 243-2272 as soon as pos- 
sible of any change in address. Note the subscription number (from the 
mailing label) and your name, old address, and new address. Allow 6 
weeks for the change. To avoid charges for replacement copies of missed is- 
sues, requests must be made within 60 days in the US and 90 days in other 
countries. 

MANUSCRIPTS. The Journal publishes clinical studies, method/device 
evaluations, reviews, and other materials related to cardiopulmonary med- 
icine and research. Manuscripts may be submitted to the Editorial Office, RES- 
PIRATORY CARE, 600 Ninth Avenue, Suite 702, Seatde WA 98104. In- 
structions for authors are printed in every issue. An expanded version of 
the Instructions is available from the editorial office. 

Copyright <D IWfi. hy Dcicihthis Enu-rpriscs hw. 



600 



RE.SPIRATORY CARE • JULY 1998 VOL 43 NO 7 



ild KJuS-Wdrnf' 





Unlike 



■W 



anything 

you've ever 

seen before, ti 

Eagle is an 

engineering 

maiyel that adds 

to the Uni'Vent 

list'Of-accomplishments ! 

Imagine a self contained^ 
battery-powered portable 
ventilator/contDressor/blender 
weighing justW^r 12-poundSy 
with a graphidffyisplay, 
powerful monitors and alarms, 
an interactive demo/teachins 
mode, and fast startup seqiik, 
that allows you to begin 
operation in as few as thn 
steps. See one now! 

OWI?£\@J Instrumentation, Inc. 

27 Fairfield Place, West Caldwe ll, NJ 0700& 
Tel. 201.882.1212 Fax. 







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Its easy to see why TheraPEF is becominj 
the PEP therapy device of choice. 



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Easy to use. 

COPD patients can master Positive Expiratory Pressure therapy quickly, and maintain an effective continuum of care away from hospital. 
TheraPEP improves secretion clearance, facilitates opening of airv^^ays and may be used for the treatment of atelectasis. 

Easy to tolerate. 

TheraPEP may reduce the need for postural drainage, and is ideal for patients unable to tolerate conventional chest physiotherapy 

Easy to read. 

Highly visible pressure indicator provides immediate, visual feedback from any angle. 

Easy to adjust. 

Slx fixed orifice options allow physicians to prescribe appropriate flow resistance levels for each patient. 

Easy to carry. 

Draw-string bag lets patients carry TheraPEP convemently and discreetly 

Easy to clean. 

Durable plastic construction, removable base, and linear, valved resistor promotes easy cleaning. 

Easy to order. 

To order your TheraPEP or a free catalog of DHD qualit)' respiratory care products, call toll-free today 

1-800-847-8000 



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Cm. t.i. NYIlni: USA (.115) (>'I7-222I FAX; (.llli) (i')7-S08.? 

CiiMniiB-r S.TM,.- I-AX I.IIS) (,'17-SI'll lill|,: '/vvvnnllld com 

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